Correction: Beyond survival to domination: Brucella's multilayered strategies for evading host immune responses

Zhimeng Wei^1,2Shuai Zhang¹Xingya Wang¹Jie Bai³Hui Wang¹Yuanchao Yang¹Jingbo Zhai^1,4,5*

• ¹School of Basic Medical Sciences, Inner Mongolia Minzu University, tongliao, China
• ²Department of Clinical Laboratory, Keerqin District First People’s Hospital, tongliao, China
• ³Department of Polyclinics, Tongliao City Center for Disease Control and Prevention, tongliao, China
• ⁴Brucellosis Prevention and Treatment Engineering Research Center of Inner Mongolia Autonomous region, Tongliao, China
• ⁵Key Laboratory of Zoonose Prevention and Control at Universities of Inner Mongolia Autonomous Region, Tongliao, China

The reference for [Bialer et al.,2020;Martín-Martín et al., 2008] was erroneously written as [Bialer, M. G., Sycz, G., Muñoz González, F., Ferrero, M., and Baldi, P. (2020). Adhesins of Brucella: Their roles in the interaction with the host. Pathogens 9:942. doi: 10.3390/pathogens9110942; Martín-Martín, A. I., Caro-Hernández, P., Orduña, A., Vizcaíno, N., and Fernández-Lago, L. (2008). Importance of the Omp25/Omp31 family in the internalization and intracellular replication of virulent B. ovis in murine macrophages and HeLa cells. Microbes Infect. 10, 706-710. doi: 10.1016/j.micinf.2008. 02.013]. It should be [Bialer, M. G., Sycz, G., Muñoz González, F., Ferrero, M., and Baldi, P. (2020). Adhesins of Brucella: Their roles in the interaction with the host. Pathogens 9:942. doi: 10.3390/pathogens9110942; Fernandez-Prada, C., Zelazowska, E., Nikolich, M., Hadfield, T., Roop, R., Robertson, G., et al. (2003). Interactions between Brucella melitensis and human phagocytes: Bacterial surface O-Polysaccharide inhibits phagocytosis, bacterial killing, and subsequent host cell apoptosis. Infect. Immun. 71, 2110-2119. doi: 10.1128/IAI.71. 4.2110-2119.2003]. The original version of this article has been updated.The reference for [Atluri et al.,2011;Lee et al.,2014] was erroneously written as [Atluri, V., Xavier, M., de Jong, M., den Hartigh, A., and Tsolis, R. (2011). Interactions of the human pathogenic Brucella species with their hosts. Annu. Rev. Microbiol. 65, 523-541. doi: 10.1146/annurev-micro-090110-102905; Lee, J., Kim, J., Kim, D., Kim, D., Simborio, H., Min, W., et al. (2014). Characterization of betaine aldehyde dehydrogenase (BetB) as an essential virulence factor of Brucella abortus. Vet. Microbiol. 168, 131-140. doi: 10.1016Microbiol. 168, 131-140. doi: 10. /j.vetmic.2013.10. 007.10. 007]. It should be [Atluri, V., Xavier, M., de Jong, M., den Hartigh, A., and Tsolis, R. (2011). Interactions of the human pathogenic Brucella species with their hosts. Annu. Rev. Microbiol. 65, 523-541. doi: 10.1146/annurev-micro-090110-102905;Barquero-Calvo, E., Chaves-Olarte, E., Weiss, D., Guzmán-Verri, C., Chacón-Díaz, C., Rucavado, A., et al. (2007). Brucella abortus uses a stealthy strategy to avoid activation of the innate immune system during the onset of infection. PLoS One 2:e631. doi: 10.1371/journal.pone.0000631]. The original version of this article has been updated.The reference for [Halling, 1998] was erroneously written as [Halling, S. (1998). On the presence and organization of open reading frames of the nonmotile pathogen Brucella abortus similar to class II, III, and IV flagellar genes and to LcrD virulence superfamily. Microb. Comp. Genom. 3, 21-29. doi: 10.1089/omi.1. 1998.3.21]. It should be [Martín-Martín, A. I., Caro-Hernández, P., Orduña, A., Vizcaíno, N., and Fernández-Lago, L. (2008). Importance of the Omp25/Omp31 family in the internalization and intracellular replication of virulent B. ovis in murine macrophages and HeLa cells. Microbes Infect. 10, 706-710. doi: 10.1016/j.micinf.2008. 02.013]. The original version of this article has been updated.The reference for [Roop et al. (2021)] was erroneously written as [Roop, R. M., Barton, I. S., Hopersberger, D., and Martin, D. (2021). Uncovering the hidden credentials of Brucella virulence. Microbiol. Mol. Biol. Rev. 85, 1-3. doi: 10.1128/mmbr.00021-19]. It should be [Halling, S. (1998). On the presence and organization of open reading frames of the nonmotile pathogen Brucella abortus similar to class II, III, and IV flagellar genes and to LcrD virulence superfamily. Microb. Comp. Genom. 3, 21-29. doi: 10.1089/omi.1. 1998.3.21]. The original version of this article has been updated.The reference for [Fretin et al., 2005] was erroneously written as [Fretin, D., Fauconnier, A., Köhler, S., Halling, S., Léonard, S., Nijskens, C., et al. (2005). The sheathed flagellum of Brucella melitensis is involved in persistence in a murine model of infection. Cell. Microbiol. 7, 687-698. doi: 10.1111/j.1462-5822.2005. 00502.x]. It should be [Roop, R. M., Barton, I. S., Hopersberger, D., and Martin, D. (2021). Uncovering the hidden credentials of Brucella virulence. Microbiol. Mol. Biol. Rev. 85, 1-3. doi: 10.1128/mmbr.00021-19]. The original version of this article has been updated.The reference for [Terwagne et al., 2013] was erroneously written as [Terwagne, M., Ferooz, J., Rolán, H., Sun, Y., Atluri, V., Xavier, M., et al. (2013). Innate immune recognition of flagellin limits systemic persistence of Brucella. Cell. Microbiol. 15, 942-960. doi: 10.1111/cmi.12088]. It should be [Fretin, D., Fauconnier, A., Köhler, S., Halling, S., Léonard, S., Nijskens, C., et al. (2005). The sheathed flagellum of Brucella melitensis is involved in persistence in a murine model of infection. Cell. Microbiol. 7, 687-698. doi: 10.1111/j.1462-5822.2005. 00502.]. The original version of this article has been updated.The reference for [Bhardwaj et al., 2021] was erroneously written as [Bhardwaj, A., Sita, K., Sehgal, A., Bhandari, K., Kumar, S., Prasad, P., et al. (2021). Heat priming of lentil (Lens culinaris Medik.) Seeds and foliar treatment with γ-aminobutyric acid (GABA), confers protection to reproductive function and yield traits under hightemperature stress environments. Int. J. Mol. Sci. 22:5825. doi: 10. 3390/ijms22115825]. It should be [Terwagne, M., Ferooz, J., Rolán, H., Sun, Y., Atluri, V., Xavier, M., et al. (2013). Innate immune recognition of flagellin limits systemic persistence of Brucella. Cell. Microbiol. 15, 942-960. doi: 10.1111/cmi.12088]. The original version of this article has been updated.The reference for [de Figueiredo et al., 2015;Spera et al., 2018] was erroneously written as [de Figueiredo, P., Ficht, T., Rice-Ficht, A., Rossetti, C., and Adams, L. (2015). Pathogenesis and immunobiology of brucellosis: Review of Brucellahost interactions. Am. J. Pathol. 185, 1505Pathol. 185, -1517Pathol. 185, . doi: 10.1016Pathol. 185, /j.ajpath.2015. 03.003;. 03.003;Spera, J. M., Guaimas, F., Corvi, M. M., and Ugalde, J. (2018). Brucella hijacks hostmediated palmitoylation to stabilize and localize PrpA to the plasma membrane. Infect. Immun. 86:e00402-18. doi: 10.1128/IAI.00402-18]. It should be [Zheng, M., Lin, R., Zhu, J., Dong, Q., Chen, J., Jiang, P., et al. (2024). Effector proteins of type IV secretion system: Weapons of Brucella used to fight against host immunity. Curr. Stem Cell. Res. Ther. 19, 145-153. doi: 10.2174/ 1574888X18666230222124529; Xiong X, Li B, Zhou Z, Gu G, Li M, Liu J, Jiao H (2021) The VirB System Plays a Crucial Role in Brucella Intracellular Infection . Int J Mol Sci, 22:24 doi: 10.3390/ijms222413637].The original version of this article has been updated.The reference for [Spera et al., 2018] was erroneously written as [Spera, J. M., Guaimas, F., Corvi, M. M., and Ugalde, J. (2018). Brucella hijacks hostmediated palmitoylation to stabilize and localize PrpA to the plasma membrane. Infect. Immun. 86:e00402-18. doi: 10.1128/IAI.00402-18]. It should be [Xiong X, Li B, Zhou Z, Gu G, Li M, Liu J, Jiao H (2021) The VirB System Plays a Crucial Role in Brucella Intracellular Infection . Int J Mol Sci, 22:24 doi: 10.3390/ijms222413637]. The original version of this article has been updated.The reference for [de Figueiredo et al., 2015;Jansen et al., 2020;Spera et al., 2018;Bergé et al.,2017] was erroneously written as [de Figueiredo, P., Ficht, T., Rice-Ficht, A., Rossetti, C., and Adams, L. (2015). Pathogenesis and immunobiology of brucellosis: Review of Brucellahost interactions. Am. J. Pathol. 185, 1505Pathol. 185, -1517Pathol. 185, . doi: 10.1016Pathol. 185, /j.ajpath.2015. 03. 03.003; Jansen, W., Demars, A., Nicaise, C., Godfroid, J., de Bolle, X., Reboul, A., et al. (2020). Shedding of Brucella melitensis happens through milk macrophages in the murine model of infection. Sci. Rep. 10:9421. doi: 10.1038/s41598-020-65760-0; Spera, J. M., Guaimas, F., Corvi, M. M., and Ugalde, J. (2018). Brucella hijacks hostmediated palmitoylation to stabilize and localize PrpA to the plasma membrane. Infect. Immun. 86:e00402-18. doi: 10.1128/IAI.00402-18;Bergé, C., Waksman, G., and Terradot, L. (2017). Structural and molecular biology of type IV secretion systems. Curr. Top. Microbiol. Immunol. 413, 31-60. doi: 10.1007/ 978-3-319-75241-9_2]. It should be [Zheng, M., Lin, R., Zhu, J., Dong, Q., Chen, J., Jiang, P., et al. (2024). Effector proteins of type IV secretion system: Weapons of Brucella used to fight against host immunity. Curr. Stem Cell. Res. Ther. 19,[145][146][147][148][149][150][151][152][153]2174/ 1574888X18666230222124529; Myeni, S., Child, R., Ng, T., Kupko, J., Wehrly, T., Porcella, S., et al. (2013). Brucella modulates secretory trafficking via multiple type IV secretion effector proteins. PLoS Pathog. 9:e1003556. doi: 10.1371/journal.ppat.1003556; Xiong X, Li B, Zhou Z, Gu G, Li M, Liu J, Jiao H (2021) The VirB System Plays a Crucial Role in Brucella Intracellular Infection . Int J Mol Sci, 22:24 doi: 10.3390/ijms222413637; Spera, J. M., Guaimas, F., Corvi, M. M., and Ugalde, J. (2018). Brucella hijacks hostmediated palmitoylation to stabilize and localize PrpA to the plasma membrane. Infect. Immun. 86:e00402-18. doi: 10.1128/IAI.00402-18]. The original version of this article has been updated.The reference for [Jansen et al., 2020] was erroneously written as [Jansen, W., Demars, A., Nicaise, C., Godfroid, J., de Bolle, X., Reboul, A., et al. (2020). Shedding of Brucella melitensis happens through milk macrophages in the murine model of infection. Sci. Rep. 10:9421. doi: 10.1038/s41598-020-65760-0]. It should be [Myeni, S., Child, R., Ng, T., Kupko, J., Wehrly, T., Porcella, S., et al. (2013). Brucella modulates secretory trafficking via multiple type IV secretion effector proteins. PLoS Pathog. 9:e1003556. doi : 10.1371/journal.ppat.1003556]. The original version of this article has been updated.The reference for [Spera et al., 2018] was erroneously written as [Spera, J. M., Guaimas, F., Corvi, M. M., and Ugalde, J. (2018). Brucella hijacks hostmediated palmitoylation to stabilize and localize PrpA to the plasma membrane. Infect. Immun. 86:e00402-18. doi: 10.1128/IAI.00402-18]. It should be [Xiong X, Li B, Zhou Z, Gu G, Li M, Liu J, Jiao H (2021) The VirB System Plays a Crucial Role in Brucella Intracellular Infection . Int J Mol Sci, 22:24 doi: 10.3390/ijms222413637]. The original version of this article has been updated.The reference for [Spera et al., 2018] was erroneously written as [Spera, J. M., Guaimas, F., Corvi, M. M., and Ugalde, J. (2018). Brucella hijacks hostmediated palmitoylation to stabilize and localize PrpA to the plasma membrane. Infect. Immun. 86:e00402-18. doi: 10.1128/IAI.00402-18]. It should be [Xiong X, Li B, Zhou Z, Gu G, Li M, Liu J, Jiao H (2021) The VirB System Plays a Crucial Role in Brucella Intracellular Infection . Int J Mol Sci, 22:24 doi: 10.3390/ijms222413637]. 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M., Guaimas, F., Corvi, M. M., and Ugalde, J. (2018). Brucella hijacks hostmediated palmitoylation to stabilize and localize PrpA to the plasma membrane. Infect. Immun. 86:e00402-18. doi: 10.1128/IAI.00402-18;Zupan, J., Hackworth, C., Aguilar, J., Ward, D., and Zambryski, P. (2007). VirB1 * promotes T-pilus formation in the vir-Type IV secretion system of Agrobacterium tumefaciens. J. Bacteriol. 189, 6551-6563. doi: 10.1128/JB.00480-07]. It should be [Xiong X, Li B, Zhou Z, Gu G, Li M, Liu J, Jiao H (2021) The VirB System Plays a Crucial Role in Brucella Intracellular Infection . Int J Mol Sci, 22:24 doi: 10.3390/ijms222413637;Ward, D., Draper, O., Zupan, J., and Zambryski, P. (2002). Peptide linkage mapping of the Agrobacterium tumefaciens vir-encoded type IV secretion system reveals protein subassemblies. Proc. Natl. Acad. Sci. U.S. A. 99, 11493-11500. doi: 10.1073/pnas. 172390299]. 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The original version of this article has been updated.The reference for [Thanassi et al., 2012;Figure 1] was erroneously written as [Thanassi, D., Bliska, J., and Christie, P. (2012). Surface organelles assembled by secretion systems of Gram-negative bacteria: Diversity in structure and function. FEMS Microbiol. Rev. 36, 1046-1082. doi: 10.1111/j.1574-6976.2012.00342.x]. It should be [Bergé, C., Waksman, G., and Terradot, L. (2017). Structural and molecular biology of type IV secretion systems. Curr. Top. Microbiol. Immunol. 413, 31-60. doi: 10.1007/ 978-3-319-75241-9_2]. The original version of this article has been updated.The reference for [Spera et al., 2018] was erroneously written as [Spera, J. M., Guaimas, F., Corvi, M. M., and Ugalde, J. (2018). Brucella hijacks hostmediated palmitoylation to stabilize and localize PrpA to the plasma membrane. Infect. Immun. 86:e00402-18. doi: 10.1128/IAI.00402-18]. It should be [Xiong X, Li B, Zhou Z, Gu G, Li M, Liu J, Jiao H (2021) The VirB System Plays a Crucial Role in Brucella Intracellular Infection . Int J Mol Sci, 22:24 doi: 10.3390/ijms222413637]. The original version of this article has been updated.The reference for [Kaplan-Türköz et al., 2013] was erroneously written as [Kaplan-Türköz, B., Koelblen, T., Felix, C., Candusso, M., O'Callaghan, D., Vergunst, A., et al. (2013). Structure of the Toll/interleukin 1 receptor (TIR) domain of the immunosuppressive Brucella effector BtpA/Btp1/TcpB. FEBS Lett. 587, 3412-3416. doi: 10.1016Lett. 587, 3412-3416. doi: 10. /j.febslet.2013.09.007.09.007]. It should be [Ellis, N., and Machner, M. (2024). Genetic approaches for identifying and characterizing effectors in bacterial pathogens. Annu. Rev. Genet. 58, 233-247. doi: 10.1146/annurev-genet-111523-102030]. The original version of this article has been updated.The reference for [Fernandez-Prada et al., 2003;Spera et al., 2018;Smith et al., 2020] was erroneously written as [Fernandez-Prada, C., Zelazowska, E., Nikolich, M., Hadfield, T., Roop, R., Robertson, G., et al. (2003). Interactions between Brucella melitensis and human phagocytes: Bacterial surface O-Polysaccharide inhibits phagocytosis, bacterial killing, and subsequent host cell apoptosis. Infect. Immun. 71, 2110-2119. doi: 10.1128/IAI.71. 4.2110-2119.2003;Spera, J. M., Guaimas, F., Corvi, M. M., and Ugalde, J. (2018). Brucella hijacks hostmediated palmitoylation to stabilize and localize PrpA to the plasma membrane. Infect. Immun. 86:e00402-18. doi: 10.1128/IAI.00402-18;Smith, E. P., Cotto-Rosario, A., Borghesan, E., Held, K., Miller, C., and Celli, J. (2020). 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The original version of this article has been updated.The reference for [de Jong et al.,2013] was erroneously written as [de Jong, M. F., Starr, T., Winter, M. G., den Hartigh, A., Child, R., Knodler, L., et al. (2013). Sensing of bacterial type IV secretion via the unfolded protein response. mBio 4:e00418-12. doi: 10.1128/mBio.00418-12]. It should be [Smith, E. P., Cotto-Rosario, A., Borghesan, E., Held, K., Miller, C., and Celli, J. (2020). Epistatic interplay between Type IV secretion effectors engages the small GTPase Rab2 in the Brucella intracellular cycle. mBio 11:e003350-19. doi: 10.1128/ mBio.03350-19]. The original version of this article has been updated.The reference for [Keestra-Gounder et al., 2016;Zhi et al., 2019;Figure 2] was erroneously written as [Keestra-Gounder, A., Byndloss, M., Seyffert, N., Young, B., Chávez-Arroyo, A., Tsai, A., et al. (2016). NOD1 and NOD2 signalling links ER stress with inflammation. Nature 532, 394-397. doi: 10.1038/nature17631;Zhi, F., Zhou, D., Bai, F., Li, J., Xiang, C., Zhang, G., et al. (2019). VceC mediated IRE1 pathway and inhibited CHOP-induced apoptosis to support Brucella replication in goat trophoblast cells. Int. J. Mol. Sci. 20:4104. doi: 10.3390/ijms20174104]. It should be [de Jong, M. F., Starr, T., Winter, M. G., den Hartigh, A., Child, R., Knodler, L., et al. (2013). Sensing of bacterial type IV secretion via the unfolded protein response. mBio 4:e00418-12. doi: 10.1128/mBio.00418-12; Keestra-Gounder, A., Byndloss, M., Seyffert, N., Young, B., Chávez-Arroyo, A., Tsai, A., et al. (2016). NOD1 and NOD2 signalling links ER stress with inflammation. Nature 532, 394-397. doi: 10.1038/nature17631]. The original version of this article has been updated.The reference for [Keestra-Gounder et al.,2016] was erroneously written as [Keestra-Gounder, A., Byndloss, M., Seyffert, N., Young, B., Chávez-Arroyo, A., Tsai, A., et al. (2016). NOD1 and NOD2 signalling links ER stress with inflammation. Nature 532, 394-397. doi: 10.1038/nature17631]. It should be [de Jong, M. F., Starr, T., Winter, M. G., den Hartigh, A., Child, R., Knodler, L., et al. (2013). Sensing of bacterial type IV secretion via the unfolded protein response. mBio 4:e00418-12. doi: 10.1128/mBio.00418-12]. The original version of this article has been updated.The reference for [Keestra-Gounder et al.,2016] was erroneously written as [Keestra-Gounder, A., Byndloss, M., Seyffert, N., Young, B., Chávez-Arroyo, A., Tsai, A., et al. (2016). NOD1 and NOD2 signalling links ER stress with inflammation. Nature 532, 394-397. doi: 10.1038/nature17631]. It should be [de Jong, M. F., Starr, T., Winter, M. G., den Hartigh, A., Child, R., Knodler, L., et al. (2013). Sensing of bacterial type IV secretion via the unfolded protein response. mBio 4:e00418-12. doi: 10.1128/mBio.00418-12]. The original version of this article has been updated.The reference for [Zhang et al., 2019] was erroneously written as [Zhang, J., Li, M., Li, Z., Shi, J., Zhang, Y., Deng, X., et al. (2019). Deletion of the type IV secretion system effector VceA promotes autophagy and inhibits apoptosis in Brucellainfected human trophoblast Cells. Curr. Microbiol. 76, 510-519. doi: 10.1007/ s00284-019-01651-6]. It should be [Zhi, F., Zhou, D., Bai, F., Li, J., Xiang, C., Zhang, G., et al. (2019). VceC mediated IRE1 pathway and inhibited CHOP-induced apoptosis to support Brucella replication in goat trophoblast cells. Int. J. Mol. Sci. 20:4104. doi: 10.3390/ijms20174104]. The original version of this article has been updated.The reference for [Gómez et al.,2020] was erroneously written as [Gómez, L., Alvarez, F., Molina, R., Soto-Shara, R., Daza-Castro, C., Flores, M., et al. (2020). A Zinc-Dependent metalloproteinase of Brucella abortus is required in the intracellular adaptation of macrophages. 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Subversion of innate immune responses by Brucella through the targeted degradation of the TLR signaling adapter. MAL J. Immunol. 184, 956-964. doi: 10.4049/jimmunol. 0902008]. The original version of this article has been updated.The reference for [Coronas-Serna et al. (2020)] was erroneously written as [Coronas-Serna, J., Louche, A., Rodríguez-Escudero, M., Roussin, M., Imbert, P., Rodríguez-Escudero, I., et al. (2020). The TIR-domain containing effectors BtpA and BtpB from Brucella abortus impact NAD metabolism. PLoS Pathog. 16:e1007979. doi: 10.1371/journal.ppat.1007979]. It should be [Dimitrakopoulos, O., Liopeta, K., Dimitracopoulos, G., and Paliogianni, F. (2013). Replication of Brucella melitensis inside primary human monocytes depends on mitogen activated protein kinase signaling. Microbes Infect. 15, 450-460. doi: 10.1016Infect. 15, 450-460. doi: 10. / j.micinf.2013.04.007].04.007]. The original version of this article has been updated.The reference for [Spera et al., 2018] was erroneously written as [Spera, J. M., Guaimas, F., Corvi, M. M., and Ugalde, J. (2018). Brucella hijacks hostmediated palmitoylation to stabilize and localize PrpA to the plasma membrane. Infect. Immun. 86:e00402-18. doi: 10.1128 The reference for [Miller et al., 2017] was erroneously written as [Miller, C., Smith, E., Cundiff, J., Knodler, L., Bailey Blackburn, J., Lupashin, V., et al. (2017). A Brucella type IV effector targets the COG Tethering complex to remodel host secretory traffic and promote intracellular replication. Cell Host Microbe 22: 317-329.e7. doi: 10.1016/j.chom.2017.07.017]. It should be [Coronas-Serna, J., Louche, A., Rodríguez-Escudero, M., Roussin, M., Imbert, P., Rodríguez-Escudero, I., et al. (2020). The TIR-domain containing effectors BtpA and BtpB from Brucella abortus impact NAD metabolism. PLoS Pathog. 16:e1007979. doi: 10.1371/journal.ppat.1007979]. The original version of this article has been updated.The reference for [Jansen et al., 2020] was erroneously written as [Jansen, W., Demars, A., Nicaise, C., Godfroid, J., de Bolle, X., Reboul, A., et al. (2020). Shedding of Brucella melitensis happens through milk macrophages in the murine model of infection. Sci. Rep. 10:9421. doi: 10.1038/s41598-020-65760-0]. It should be [Myeni, S., Child, R., Ng, T., Kupko, J., Wehrly, T., Porcella, S., et al. (2013). Brucella modulates secretory trafficking via multiple type IV secretion effector proteins. PLoS Pathog. 9:e1003556. doi : 10.1371/journal.ppat.1003556]. The original version of this article has been updated.The reference for [Borghesan et al., 2021] was erroneously written as [Borghesan, E., Smith, E., Myeni, S., Binder, K., Knodler, L., and Celli, J. A. (2021). Brucella effector modulates the Arf6-Rab8a GTPase cascade to promote intravacuolar replication. EMBO J. 40:e107664. doi: 10.15252/embj.2021107664]. It should be [Miller, C., Smith, E., Cundiff, J., Knodler, L., Bailey Blackburn, J., Lupashin, V., et al. (2017). A Brucella type IV effector targets the COG Tethering complex to remodel host secretory traffic and promote intracellular replication. Cell Host Microbe 22:317-329.e7. doi: 10.1016/j.chom.2017.07.017]. The original version of this article has been updated.The reference for [Lin et al., 2023] was erroneously written as [Lin, R., Li, A., Li, Y., Shen, R., Du, F., Zheng, M., et al. (2023). The Brucella effector protein BspF regulates apoptosis through the crotonylation of p53. Microorganisms 11:2322. doi: 10.3390/microorganisms11092322]. It should be [Borghesan, E., Smith, E., Myeni, S., Binder, K., Knodler, L., and Celli, J. A. (2021). Brucella effector modulates the Arf6-Rab8a GTPase cascade to promote intravacuolar replication. EMBO J. 40:e107664. doi: 10.15252/embj.2021107664]. The original version of this article has been updated.The reference for [Marchesini et al., 2016] was erroneously written as [Marchesini, M. I., Morrone Seijo, S. M., Guaimas, F. F., and Comerci, D. (2016). A T4SS effector targets host cell alpha-enolase contributing to Brucella abortus intracellular lifestyle. Front. Cell. Infect. Microbiol. 6:153. doi: 10.3389/fcimb.2016. 00153]. It should be [Lin, R., Li, A., Li, Y., Shen, R., Du, F., Zheng, M., et al. (2023). The Brucella effector protein BspF regulates apoptosis through the crotonylation of p53. Microorganisms 11:2322. doi: 10.3390/microorganisms11092322]. The original version of this article has been updated.The reference for [Döhmer et al., 2014] was erroneously written as [Döhmer, P., Valguarnera, E., Czibener, C., and Ugalde, J. (2014). Identification of a type IV secretion substrate of Brucella abortus that participates in the early stages of intracellular survival. Cell. Microbiol. 16, 396-410. doi: 10.1111/cmi.12224]. It should be [Marchesini, M. I., Morrone Seijo, S. M., Guaimas, F. F., and Comerci, D. (2016). A T4SS effector targets host cell alpha-enolase contributing to Brucella abortus intracellular lifestyle. Front. Cell. Infect. Microbiol. 6:153. doi: 10.3389/fcimb.2016. 00153]. The original version of this article has been updated.The reference for [de Figueiredo et al., 2015;Luizet et al., 2021] was erroneously written as [de Figueiredo, P., Ficht, T., Rice-Ficht, A., Rossetti, C., and Adams, L. (2015). Pathogenesis and immunobiology of brucellosis: Review of Brucellahost interactions. Am. J. Pathol. 185, 1505Pathol. 185, -1517Pathol. 185, . doi: 10.1016Pathol. 185, /j.ajpath.2015. 03.003;. 03.003;Luizet, J. B., Raymond, J., Lacerda, T. L., Barbieux, E., Kambarev, S., Bonici, M., et al. (2021). The Brucella effector BspL targets the ER-associated degradation (ERAD) pathway and delays bacterial egress from infected cells. Proc. Natl. Acad. Sci. 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The Brucella effector BspI suppresses inflammation via inhibition of IRE1 kinase activity during Brucella infection. J. Immunol. 209, 488-497. doi: 10.4049/jimmunol.2200001]. It should be [Louche, A., Blanco, A., Lacerda, T., Cancade-Veyre, L., Lionnet, C., Bergé, C., et al. (2023). Brucella effectors NyxA and NyxB target SENP3 to modulate the subcellular localisation of nucleolar proteins. Nat. Commun. 14:102. doi: 10.1038/s41467-022-35763-8]. The original version of this article has been updated.The reference for [Sengupta et al.,2010] was erroneously written as [Sengupta, D., Koblansky, A., Gaines, J., Brown, T., West, A., Zhang, D., et al. (2010). Subversion of innate immune responses by Brucella through the targeted degradation of the TLR signaling adapter. MAL J. Immunol. 184, 956-964. doi: 10.4049/jimmunol. 0902008]. It should be [Hashemifar, I., Yadegar, A., Jazi, F., and Amirmozafari, N. (2017). Molecular prevalence of putative virulence-associated genes in Brucella melitensis and Brucella abortus isolates from human and livestock specimens in Iran. Microb. Pathog. 105, 334-339. doi: 10.1016/j.micpath.2017.03.007]. The original version of this article has been updated.The reference for [Ma et al., 2020] was erroneously written as [Ma, Z., Li, R., Hu, R., Deng, X., Xu, Y., Zheng, W., et al. (2020). Brucella abortus BspJ is a nucleomodulin that inhibits macrophage apoptosis and promotes intracellular survival of Brucella. Front. Microbiol. 11:599205. doi: 10.3389/fmicb.2020.599205]. It should be [Li, C., Wang, J., Sun, W., Liu, X., Wang, J., and Peng, Q. (2022). The Brucella effector BspI suppresses inflammation via inhibition of IRE1 kinase activity during Brucella infection. J. Immunol. 209, 488-497. doi: 10.4049/jimmunol.2200001]. The original version of this article has been updated.The reference for [Giménez et al.,2024] was erroneously written as [Giménez, A., Del Giudice, M., López, P., Guaimas, F., Sámano-Sánchez, H., Gibson, T., et al. (2024). Brucella NpeA is a secreted Type IV effector containing an N-WASPbinding short linear motif that promotes niche formation. mBio 15:e00726-24. doi: 10.1128/mbio.00726-24]. It should be [Ma, Z., Li, R., Hu, R., Deng, X., Xu, Y., Zheng, W., et al. (2020). Brucella abortus BspJ is a nucleomodulin that inhibits macrophage apoptosis and promotes intracellular survival of Brucella. Front. Microbiol. 11:599205. doi: 10.3389/fmicb.2020.599205]. The original version of this article has been updated.The reference for [Yin et al., 2024] was erroneously written as [Yin, Y., Tian, M., Zhang, G., Hu, H., Ding, C., and Yu, S. (2024). Identification of Brucella RS15060 as a novel type IV secretion system effector associated with bacterial virulence. Vet. Res. 55:168. doi: 10.1186/s13567-024-01417-4]. It should be [Giménez, A., Del Giudice, M., López, P., Guaimas, F., Sámano-Sánchez, H., Gibson, T., et al. (2024). Brucella NpeA is a secreted Type IV effector containing an N-WASPbinding short linear motif that promotes niche formation. mBio 15:e00726-24. doi: 10.1128/mbio.00726-24]. The original version of this article has been updated.The reference for [Yin et al., 2025] was erroneously written as [Yin, Y., Tian, M., Zhang, G., Ding, C., and Yu, S. A. (2025). novel Brucella T4SS effector RS15060 acts on bacterial morphology, lipopolysaccharide core synthesis and host proinflammatory responses, which is beneficial for Brucella melitensis virulence. Microbiol. Res. 292:128015. doi: 10.1016/j.micres.2024.128015]. It should be [Yin, Y., Tian, M., Zhang, G., Hu, H., Ding, C., and Yu, S. (2024). Identification of Brucella RS15060 as a novel type IV secretion system effector associated with bacterial virulence. Vet. 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The effector protein bpe005 from Brucella abortus induces collagen deposition and matrix metalloproteinase 9 downmodulation via transforming growth factor β1 in hepatic stellate cells. Infect. Immun. 84, 598-606. doi: 10.1128/IAI.01227-15]. It should be [He, J., Yin, S., Deng, X., Ma, Z., Zhang, H., Miao, Y., et al. (2025). The effector protein BspE affects Brucella survival by regulating the inflammatory response and apoptosis. Int. Immunopharmacol. 144:113576. doi: 10.1016/j.intimp.2024.113576]. The original version of this article has been updated.The reference for [Spera et al., 2014] was erroneously written as [Spera, J., Comerci, D., and Ugalde, J. (2014). Brucella alters the immune response in a prpAdependent manner. Microb. Pathog. 67-68, 8-13. doi: 10.1016/j.micpath.2014. 01.003]. It should be [Arriola Benitez, P., Rey Serantes, D., Herrmann, C., Pesce Viglietti, A., Vanzulli, S., Giambartolomei, G., et al. (2016). The effector protein bpe005 from Brucella abortus induces collagen deposition and matrix metalloproteinase 9 downmodulation via transforming growth factor β1 in hepatic stellate cells. Infect. Immun. 84, 598-606. doi: 10.1128/IAI.01227-15]. The original version of this article has been updated.The reference for [Li C. et al., 2022] was erroneously written as [Li, C., Wang, J., Sun, W., Liu, X., Wang, J., and Peng, Q. (2022). The Brucella effector BspI suppresses inflammation via inhibition of IRE1 kinase activity during Brucella infection. J. Immunol. 209, 488-497. doi: 10.4049/jimmunol.2200001]. It should be [Louche, A., Blanco, A., Lacerda, T., Cancade-Veyre, L., Lionnet, C., Bergé, C., et al. (2023). Brucella effectors NyxA and NyxB target SENP3 to modulate the subcellular localisation of nucleolar proteins. Nat. Commun. 14:102. doi: 10.1038/s41467-022-35763-8]. The original version of this article has been updated.The reference for [Bergé et al., 2017] was erroneously written as [Bergé, C., Waksman, G., and Terradot, L. (2017). Structural and molecular biology of type IV secretion systems. Curr. Top. Microbiol. Immunol. 413, 31-60. doi: 10.1007/ 978-3-319-75241-9_2]. It should be [Spera, J. M., Guaimas, F., Corvi, M. M., and Ugalde, J. (2018). Brucella hijacks hostmediated palmitoylation to stabilize and localize PrpA to the plasma membrane. Infect. Immun. 86:e00402-18. doi: 10.1128/IAI.00402-18]. The original version of this article has been updated.The reference for [Bergé et al., 2017;Spera et al., 2006] was erroneously written as [Bergé, C., Waksman, G., and Terradot, L. (2017). Structural and molecular biology of type IV secretion systems. Curr. Top. Microbiol. Immunol. 413,.1007/ 978-3-319-75241-9_2; Spera, J., Ugalde, J., Mucci, J., Comerci, D., and Ugalde, R. A. (2006). A B lymphocyte mitogen is a Brucella abortus virulence factor required for persistent infection. Proc. Natl. Acad. Sci. U.S. A. 103, 16514-16519. doi: 10.1073/pnas.0603362103]. It should be [Spera, J. M., Guaimas, F., Corvi, M. M., and Ugalde, J. (2018). Brucella hijacks hostmediated palmitoylation to stabilize and localize PrpA to the plasma membrane. Infect. Immun. 86:e00402-18. doi: 10.1128/IAI.00402-18;Spera, J., Comerci, D., and Ugalde, J. (2014). Brucella alters the immune response in a prpA-dependent manner. Microb. Pathog. 67-68, 8-13. doi: 10.1016/j.micpath.2014. 01.003]. The original version of this article has been updated.The reference for [Spera et al., 2006;Liu et al., 2018] was erroneously written as [Spera, J., Ugalde, J., Mucci, J., Comerci, D., and Ugalde, R. A. (2006). A B lymphocyte mitogen is a Brucella abortus virulence factor required for persistent infection. Proc. Natl. Acad. Sci. 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Overexpression of Cu-Zn SOD in Brucella abortus suppresses bacterial intracellular replication via downregulation of Sar1 activity. Oncotarget 9, 9596-9607. doi: 10.18632/oncotarget.24073]. The original version of this article has been updated.The reference for [de Jong et al.,2013] was erroneously written as [de Jong, M. F., Starr, T., Winter, M. G., den Hartigh, A., Child, R., Knodler, L., et al. (2013). Sensing of bacterial type IV secretion via the unfolded protein response. mBio 4:e00418-12. doi: 10.1128/mBio.00418-12]. It should be [Smith, E. P., Cotto-Rosario, A., Borghesan, E., Held, K., Miller, C., and Celli, J. (2020). Epistatic interplay between Type IV secretion effectors engages the small GTPase Rab2 in the Brucella intracellular cycle. mBio 11:e003350-19. doi: 10.1128/ mBio.03350-19]. 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G., den Hartigh, A., Child, R., Knodler, L., et al. (2013). Sensing of bacterial type IV secretion via the unfolded protein response. mBio 4:e00418-12. doi: 10.1128/mBio.00418-12;Keestra-Gounder, A., Byndloss, M., Seyffert, N., Young, B., Chávez-Arroyo, A., Tsai, A., et al. (2016). NOD1 and NOD2 signalling links ER stress with inflammation. Nature 532, 394-397. doi: 10.1038/nature17631; Zhi, F., Zhou, D., Bai, F., Li, J., Xiang, C., Zhang, G., et al. (2019). VceC mediated IRE1 pathway and inhibited CHOP-induced apoptosis to support Brucella replication in goat trophoblast cells. Int. J. Mol. Sci. 20:4104. doi: 10.3390/ijms20174104]. The original version of this article has been updated.The reference for [Gómez et al.,2020] was erroneously written as [Gómez, L., Alvarez, F., Molina, R., Soto-Shara, R., Daza-Castro, C., Flores, M., et al. (2020). A Zinc-Dependent metalloproteinase of Brucella abortus is required in the intracellular adaptation of macrophages. Front. 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A Brucella type IV effector targets the COG Tethering complex to remodel host secretory traffic and promote intracellular replication. Cell Host Microbe 22:317-329.e7. doi: 10.1016/j.chom.2017.07.017]. It should be [Xiong X, Li B, Zhou Z, Gu G, Li M, Liu J, Jiao H (2021) The VirB System Plays a Crucial Role in Brucella Intracellular Infection . Int J Mol Sci, 22:24 doi: 10.3390/ijms222413637; Coronas-Serna, J., Louche, A., Rodríguez-Escudero, M., Roussin, M., Imbert, P., Rodríguez-Escudero, I., et al. (2020). The TIR-domain containing effectors BtpA and BtpB from Brucella abortus impact NAD metabolism. PLoS Pathog. 16:e1007979. doi: 10.1371/journal.ppat.1007979]. The original version of this article has been updated.The reference for [Jansen et al., 2020;de Jong et al., 2013;Borghesan et al., 2021] was erroneously written as [Jansen, W., Demars, A., Nicaise, C., Godfroid, J., de Bolle, X., Reboul, A., et al. (2020). 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The original version of this article has been updated.The reference for [Döhmer et al.,2014] was erroneously written as [Döhmer, P., Valguarnera, E., Czibener, C., and Ugalde, J. (2014). Identification of a type IV secretion substrate of Brucella abortus that participates in the early stages of intracellular survival. Cell. Microbiol. 16, 396-410. doi: 10.1111 A., Vanzulli, S., Giambartolomei, G., et al. (2016). The effector protein bpe005 from Brucella abortus induces collagen deposition and matrix metalloproteinase 9 downmodulation via transforming growth factor β1 in hepatic stellate cells. Infect. Immun. 84, 598-606. doi: 10.1128/IAI.01227-15]. The original version of this article has been updated.The reference for [Sengupta et al.,2010] was erroneously written as [Sengupta, D., Koblansky, A., Gaines, J., Brown, T., West, A., Zhang, D., et al. (2010). Subversion of innate immune responses by Brucella through the targeted degradation of the TLR signaling adapter. MAL J. Immunol. 184,[956][957][958][959][960][961][962][963][964] The reference for [Giménez et al.,2024] was erroneously written as [Giménez, A., Del Giudice, M., López, P., Guaimas, F., Sámano-Sánchez, H., Gibson, T., et al. (2024). Brucella NpeA is a secreted Type IV effector containing an N-WASPbinding short linear motif that promotes niche formation. mBio 15:e00726-24. doi: 10.1128/mbio.00726-24]. It should be [Ma, Z., Li, R., Hu, R., Deng, X., Xu, Y., Zheng, W., et al. (2020). Brucella abortus BspJ is a nucleomodulin that inhibits macrophage apoptosis and promotes intracellular survival of Brucella. Front. Microbiol. 11:599205. doi: 10.3389/fmicb.2020.599205].The original version of this article has been updated.The reference for [Li C. et al.,2022] was erroneously written as [Li, C., Wang, J., Sun, W., Liu, X., Wang, J., and Peng, Q. ( 2022). The Brucella effector BspI suppresses inflammation via inhibition of IRE1 kinase activity during Brucella infection. J. 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Immun. 67, 4960-4962. doi: 10.1128/IAI.67.9.4960-4962.1999]. The original version of this article has been updated.The reference for [Cloeckaert et al., 1996b] was erroneously written as [Cloeckaert, A., Verger, J., Grayon, M., Zygmunt, M., and Grépinet, O. (1996b). Nucleotide sequence and expression of the gene encoding the major 25-kilodalton outer membrane protein of Brucella ovis: Evidence for antigenic shift, compared with other Brucella species, due to a deletion in the gene. Infect. Immun. 64, 2047-2055. doi: 10.1128/iai.64.6.2047-2055.1996]. It should be [Cloeckaert, A., Verger, J., Grayon, M., and Vizcaíno, N. (1996a). Molecular and immunological characterization of the major outer membrane proteins of Brucella. FEMS Microbiol. Lett. 145, 1-8. doi: 10.1111Lett. 145, 1-8. doi: 10. /j.1574Lett. 145, 1-8. doi: 10. -6968.1996.tb08547.x].tb08547.x]. 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Nucleotide sequence and expression of the gene encoding the major 25-kilodalton outer membrane protein of Brucella ovis: Evidence for antigenic shift, compared with other Brucella species, due to a deletion in the gene. Infect. Immun. 64, 2047-2055. doi: 10.1128/iai.64.6.2047-2055.1996;Guzman-Verri, C., Manterola, L., Sola-Landa, A., Parra, A., Cloeckaert, A., Garin, J., et al. (2002). The two-component system BvrR/BvrS essential for Brucella abortus virulence regulates the expression of outer membrane proteins with counterparts in members of the Rhizobiaceae. Proc. Natl. Acad. Sci. U.S. A. 99, 12375-12380. doi: 10.1073/pnas.192439399]. The original version of this article has been updated.The reference for [Cloeckaert et al., 1996b] was erroneously written as [Cloeckaert, A., Verger, J., Grayon, M., Zygmunt, M., and Grépinet, O. (1996b). Nucleotide sequence and expression of the gene encoding the major 25-kilodalton outer membrane protein of Brucella ovis: Evidence for antigenic shift, compared with other Brucella species, due to a deletion in the gene. Infect. Immun. 64, 2047-2055. doi: 10.1128/iai.64.6.2047-2055.1996]. It should be [Cloeckaert, A., Verger, J., Grayon, M., and Vizcaíno, N. (1996a). Molecular and immunological characterization of the major outer membrane proteins of Brucella. FEMS Microbiol. Lett. 145, 1-8. doi: 10.1111Lett. 145, 1-8. doi: 10. /j.1574Lett. 145, 1-8. doi: 10. -6968.1996.tb08547.x].tb08547.x]. The original version of this article has been updated.The reference for [Dubray and Bézard,1980] was erroneously written as [Dubray, G., and Bézard, G. (1980). Isolation of three Brucella abortus cell-wall antigens protective in murine experimental brucellosis. Ann. Rech. Vet. 11, 367-373. doi: 10.1016/s0378-1135(02)00110-4]. 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Immunopathol. 18, 149-163. doi: 10.1016/0165-2427(88)90057-8; Edmonds, M., Cloeckaert, A., and Elzer, P. (2002). Brucella species lacking the major outer membrane protein Omp25 are attenuated in mice and protect against Brucella melitensis and Brucella ovis. Vet. Microbiol. 88,[205][206][207][208][209][210][211][212][213][214][215][216][217][218][219][220][221]1016/s0378-1135(02) 00110-4; Zhu, H., Jiao, H., Nie, X., Li, B., Xu, K., Pang, F., et al. (2018). Alterations of microRNAs and their predicted targeting mRNAs expression in RAW264.7 macrophages infected with Omp25 mutant Brucella melitensis. Innate Immun. 24, 382-389. doi: 10.1177/1753425918792298]. It should be [Dubray, G., and Bézard, G. (1980). Isolation of three Brucella abortus cell-wall antigens protective in murine experimental brucellosis. Ann. Rech. Vet. 11, 367-373. doi: 10.1016Vet. 11, 367-373. doi: 10. /s0378-1135(02)(02) 00110-4;Montaraz, J., and Winter, A. (1986). Comparison of living and nonliving vaccines for Brucella abortus in BALB/c mice. Infect. Immun. 53, 245-251. doi: 10.1128Immun. 53, 245-251. doi: 10. /iai.53. 2.245-251.1986;;Winter, A., and Rowe, G. (1988). Comparative immune responses to native cell envelope antigens and the hot sodium dodecyl sulfate insoluble fraction (PG) of Brucella abortus in cattle and mice. Vet. Immunol. Immunopathol. 18, 149-163. doi: 10.1016/0165-2427(88)90057-8;Edmonds, M., Cloeckaert, A., and Elzer, P. (2002). Brucella species lacking the major outer membrane protein Omp25 are attenuated in mice and protect against Brucella melitensis and Brucella ovis. Vet. Microbiol. 88, 205-221. doi: 10.1016Microbiol. 88, 205-221. doi: 10. /s0378-1135(02) (02) The reference for [Verdiguel-Fernández et al. (2017)] was erroneously written as [Verdiguel-Fernández, L., Oropeza-Navarro, R., Basurto-Alcántara, F., Castañeda Ramírez, A., and Verdugo-Rodríguez, A. (2017). Omp31 plays an important role on outer membrane properties and intracellular survival of Brucella melitensis in murine macrophages and HeLa cells. Arch. Microbiol. 199, 971-978. doi: 10.1007Microbiol. 199, 971-978. doi: 10. /s00203-017-1360-7-7]. It should be [Jubier-Maurin, V., Boigegrain, R., Cloeckaert, A., Gross, A., Alvarez-Martinez, M., Terraza, A., et al. (2001). Major outer membrane protein Omp25 of Brucella suis is involved in inhibition of tumor necrosis factor alpha production during infection of human macrophages. Infect. Immun. 69, 4823-4830. doi: 10.1128/IAI.69.8.4823-4830. 2001]. The original version of this article has been updated.The reference for [Verdiguel-Fernández et al. (2017)] was erroneously written as [Verdiguel-Fernández, L., Oropeza-Navarro, R., Basurto-Alcántara, F., Castañeda Ramírez, A., and Verdugo-Rodríguez, A. (2017). Omp31 plays an important role on outer membrane properties and intracellular survival of Brucella melitensis in murine macrophages and HeLa cells. Arch. Microbiol. 199, 971-978. doi: 10.1007Microbiol. 199, 971-978. doi: 10. /s00203-017-1360-7-7]. It should be [Jubier-Maurin, V., Boigegrain, R., Cloeckaert, A., Gross, A., Alvarez-Martinez, M., Terraza, A., et al. (2001). Major outer membrane protein Omp25 of Brucella suis is involved in inhibition of tumor necrosis factor alpha production during infection of human macrophages. Infect. Immun. 69, 4823-4830. doi: 10.1128/IAI.69.8.4823-4830. 2001]. The original version of this article has been updated.The reference for [Verdiguel-Fernández et al. (2017)] was erroneously written as [Verdiguel-Fernández, L., Oropeza-Navarro, R., Basurto-Alcántara, F., Castañeda Ramírez, A., and Verdugo-Rodríguez, A. ( 2017). Omp31 plays an important role on outer membrane properties and intracellular survival of Brucella melitensis in murine macrophages and HeLa cells. Arch. Microbiol. 199, 971-978. doi: 10.1007Microbiol. 199, 971-978. doi: 10. /s00203-017-1360-7-7]. It should be [Jubier-Maurin, V., Boigegrain, R., Cloeckaert, A., Gross, A., Alvarez-Martinez, M., Terraza, A., et al. (2001). Major outer membrane protein Omp25 of Brucella suis is involved in inhibition of tumor necrosis factor alpha production during infection of human macrophages. Infect. Immun. 69, 4823-4830. doi: 10.1128/IAI.69.8.4823-4830. 2001]. The original version of this article has been updated.The reference for [Delpino et al. (2006)] was erroneously written as [Delpino, M., Cassataro, J., Fossati, C., Goldbaum, F., and Baldi, P. (2006). Brucella outer membrane protein Omp31 is a haemin-binding protein. Microbes Infect. 8, 1203Infect. 8, -1208Infect. 8, . doi: 10.1016Infect. 8, /j.micinf.2005.11.11.008]. 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Activation of Rho and Rab GTPases dissociates Brucella abortus internalization from intracellular trafficking. Cell. Microbiol. 4, 663-676. doi: 10.1046Microbiol. 4, 663-676. doi: 10. /j.1462Microbiol. 4, 663-676. doi: 10. -5822.2002.00221.x].00221.x]. The original version of this article has been updated.The reference for [Comerci et al., 2001] was erroneously written as [Comerci, D., Martínez-Lorenzo, M., Sieira, R., Gorvel, J., and Ugalde, R. (2001). Essential role of the VirB machinery in the maturation of the Brucella abortuscontaining vacuole. Cell. Microbiol. 3, 159-168. doi: 10.1046/j.1462-5822.2001.00102. x]. It should be [Gross, A., Spiesser, S., Terraza, A., Rouot, B., Caron, E., and Dornand, J. (1998). Expression and bactericidal activity of nitric oxide synthase in Brucella suis-infected murine macrophages. Infect. Immun. 66, 1309-1316. doi: 10.1128/IAI.66.4.1309-1316. 1998]. 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Brucella abortus transits through the autophagic pathway and replicates in the endoplasmic reticulum of nonprofessional phagocytes. Infect. Immun. 66, 5711-5724. doi: 10.1128/IAI.66.12.5711-5724.1998;Pizarro-Cerdá, J., Moreno, E., Sanguedolce, V., Mege, J., and Gorvel, J. (1998b). Virulent Brucella abortus prevents lysosome fusion and is distributed within autophagosome-like compartments. Infect. Immun. 66, 2387-2392. doi: 10.1128/IAI. 66.5.2387-2392.1998;Starr, T., Ng, T., Wehrly, T., Knodler, L., and Celli, J. (2008). Brucella intracellular replication requires trafficking through the late endosomal/lysosomal compartment. Traffic 9, 678-694. doi: 10.1111Traffic 9, 678-694. doi: 10. /j.1600Traffic 9, 678-694. doi: 10. -0854.2008.00718.x].00718.x]. It should be [Chaves-Olarte, E., Guzmán-Verri, C., Méresse, S., Desjardins, M., Pizarro-Cerdá, J., Badilla, J., et al. (2002). Activation of Rho and Rab GTPases dissociates Brucella abortus internalization from intracellular trafficking. 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The original version of this article has been updated.The reference for [Celli, 2019;Aly and Baron, 2007;Starr et al., 2012;Fugier et al., 2009] was erroneously written as [Celli, J. (2019). The intracellular life cycle of Brucella spp. Microbiol. Spectr. 7:6. doi: 10.1128/microbiolspec.bai-0006-2019; Aly, K., and Baron, C. (2007). The VirB5 protein localizes to the T-pilus tips in Agrobacterium tumefaciens. Microbiology (Reading) 153, 3766-3775. doi: 10.1099/mic. 0.2007/010462-0; Starr, T., Child, R., Wehrly, T., Hansen, B., Hwang, S., López-Otin, C., et al. (2012). Selective subversion of autophagy complexes facilitates completion of the Brucella intracellular cycle. Cell Host Microbe 11, 33-45. doi: 10.1016Microbe 11, 33-45. doi: 10. /j.chom.2011.12.002;.12.002;Fugier, E., Salcedo, S., de Chastellier, C., Pophillat, M., Muller, A., Arce-Gorvel, V., et al. (2009). The glyceraldehyde-3phosphate dehydrogenase and the small GTPase Rab 2 are crucial for Brucella replication. 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It should be [Zhang, G., Hu, H., Yin, Y., Tian, M., Bu, Z., Ding, C., et al. (2024). Brucella manipulates host cell ferroptosis to facilitate its intracellular replication and egress in RAW264.7 macrophages. Antioxidants (Basel) 13:577. doi: 10.3390/antiox13050577]. The reference for [Li C. et al., 2022] was erroneously written as [Li, X., Zhu, Y., Zhang, X., An, X., Weng, M., Shi, J., et al. (2022). An alternatively spliced STING isoform localizes in the cytoplasmic membrane and directly senses extracellular cGAMP. J. Clin. Invest. 132:e144339. doi: 10.1172/JCI144339]. It should be [Zhang, G., Hu, H., Yin, Y., Tian, M., Bu, Z., Ding, C., et al. (2024). Brucella manipulates host cell ferroptosis to facilitate its intracellular replication and egress in RAW264.7 macrophages. Antioxidants (Basel) 13:577. doi: 10.3390/antiox13050577]. 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Immunol. 200, 607-622. doi: 10.4049/jimmunol.1700725;Burdette, D., Monroe, K., Sotelo-Troha, K., Iwig, J., Eckert, B., Hyodo, M., et al. (2011). STING is a direct innate immune sensor of cyclic di-GMP. Nature 478, 515-518. doi: 10.1038/nature10429]. The reference for [Burdette et al., 2011;Tong et al., 2024;Ishikawa et al., 2009] was erroneously written as [Burdette, D., Monroe, K., Sotelo-Troha, K., Iwig, J., Eckert, B., Hyodo, M., et al. (2011). STING is a direct innate immune sensor of cyclic di-GMP. Nature 478, 515-518. doi: 10.1038/nature10429; Tong, J., Song, J., Zhang, W., Zhai, J., Guan, Q., Wang, H., et al. (2024). When DNA-damage responses meet innate and adaptive immunity. Cell. Mol. Life Sci. 81:185. doi: 10.1007/s00018-024-05214-2; Ishikawa, H., Ma, Z., and Barber, G. N. ( 2009). STING regulates intracellular DNAmediated, type I interferon-dependent innate immunity. Nature 461, 788-792. doi: 10.1038/nature08476]. It should be [Costa Franco, M., Marim, F., Guimarães, E., Assis, N., Cerqueira, D., Alves-Silva, J., et al. (2018). Brucella abortus triggers a cGAS-independent STING pathway to induce host protection that involves guanylate-binding proteins and inflammasome activation. J. Immunol. 200, 607-622. doi: 10.4049/jimmunol.1700725;Li, X., Zhu, Y., Zhang, X., An, X., Weng, M., Shi, J., et al. (2022). An alternatively spliced STING isoform localizes in the cytoplasmic membrane and directly senses extracellular cGAMP. J. Clin. Invest. 132:e144339. doi: 10.1172/JCI144339; Tong, J., Song, J., Zhang, W., Zhai, J., Guan, Q., Wang, H., et al. (2024). When DNAdamage responses meet innate and adaptive immunity. Cell. Mol. Life Sci. 81:185. doi: 10.1007/s00018-024-05214-2]. The reference for [Burdette et al., 2011;Ishikawa et al., 2009;Chen et al., 2016;Meunier et al., 2015] was erroneously written as [Burdette, D., Monroe, K., Sotelo-Troha, K., Iwig, J., Eckert, B., Hyodo, M., et al. (2011). STING is a direct innate immune sensor of cyclic di-GMP. Nature 478, 515-518. doi: 10.1038/nature10429;Ishikawa, H., Ma, Z., and Barber, G. N. (2009). STING regulates intracellular DNAmediated, type I interferon-dependent innate immunity. Nature 461, 788-792. doi: 10.1038/nature08476; Chen, Q., Sun, L., and Chen, Z. (2016). Regulation and function of the cGAS-STING pathway of cytosolic DNA sensing. Nat. Immunol. 17, 1142-1149. doi: 10.1038/ni.3558;Meunier, E., Wallet, P., Dreier, R., Costanzo, S., Anton, L., Rühl, S., et al. (2015). Guanylate-binding proteins promote activation of the AIM2 inflammasome during infection with Francisella novicida. Nat. Immunol. 16, 476-484. doi: 10.1038/ni.3119]. It should be [Costa Franco, M., Marim, F., Guimarães, E., Assis, N., Cerqueira, D., Alves-Silva, J., et al. (2018). Brucella abortus triggers a cGAS-independent STING pathway to induce host protection that involves guanylate-binding proteins and inflammasome activation. J. Immunol. 200, 607-622. doi: 10.4049/jimmunol.1700725;Tong, J., Song, J., Zhang, W., Zhai, J., Guan, Q., Wang, H., et al. (2024). When DNA-damage responses meet innate and adaptive immunity. Cell. Mol. Life Sci. 81:185. doi: 10.1007/s00018-024-05214-2; Ishikawa, H., Ma, Z., and Barber, G. N. (2009). STING regulates intracellular DNAmediated, type I interferon-dependent innate immunity. Nature 461, 788-792. doi: 10.1038/nature08476; Chen, Q., Sun, L., and Chen, Z. ( 2016). Regulation and function of the cGAS-STING pathway of cytosolic DNA sensing. Nat. Immunol. 17, 1142-1149. doi: 10.1038/ni.3558]. The reference for [Burdette et al., 2011;Chen et al., 2016;Meunier et al., 2015] was erroneously written as [Burdette, D., Monroe, K., Sotelo-Troha, K., Iwig, J., Eckert, B., Hyodo, M., et al. (2011). STING is a direct innate immune sensor of cyclic di-GMP. Nature 478, 515-518. doi: 10.1038/nature10429; Chen, Q., Sun, L., and Chen, Z. ( 2016). Regulation and function of the cGAS-STING pathway of cytosolic DNA sensing. Nat. Immunol. 17, 1142-1149. doi: 10.1038/ni.3558;Meunier, E., Wallet, P., Dreier, R., Costanzo, S., Anton, L., Rühl, S., et al. (2015). Guanylate-binding proteins promote activation of the AIM2 inflammasome during infection with Francisella novicida. Nat. Immunol. 16, 476-484. doi: 10.1038/ni.3119]. It should be [Costa Franco, M., Marim, F., Guimarães, E., Assis, N., Cerqueira, D., Alves-Silva, J., et al. (2018). Brucella abortus triggers a cGASindependent STING pathway to induce host protection that involves guanylatebinding proteins and inflammasome activation. J. Immunol. 200, 607-622. doi: 10.4049/jimmunol.1700725;Ishikawa, H., Ma, Z., and Barber, G. N. (2009). STING regulates intracellular DNAmediated, type I interferon-dependent innate immunity. Nature 461, 788-792. doi: 10.1038/nature08476; Chen, Q., Sun, L., and Chen, Z. (2016). Regulation and function of the cGAS-STING pathway of cytosolic DNA sensing. Nat. Immunol. 17, 1142-1149. doi: 10.1038/ni.3558]. The reference for [Burdette et al., 2011;Figure 2] was erroneously written as [Burdette, D., Monroe, K., Sotelo-Troha, K., Iwig, J., Eckert, B., Hyodo, M., et al. (2011). STING is a direct innate immune sensor of cyclic di-GMP. Nature 478, 515-518. doi: 10.1038/nature10429]. It should be [Costa Franco, M., Marim, F., Guimarães, E., Assis, N., Cerqueira, D., Alves-Silva, J., et al. (2018). Brucella abortus triggers a cGAS-independent STING pathway to induce host protection that involves guanylate-binding proteins and inflammasome activation. J. Immunol. 200, 607-622. doi: 10.4049/jimmunol.1700725]. The reference for [Burdette et al., 2011;Gomes et al., 2021] was erroneously written as [Burdette, D., Monroe, K., Sotelo-Troha, K., Iwig, J., Eckert, B., Hyodo, M., et al. (2011). STING is a direct innate immune sensor of cyclic di-GMP. Nature 478, 515-518. doi: 10.1038/nature10429;Gomes, M., Guimarães, E., Marinho, F., Macedo, I., Aguiar, E., Barber, G., et al. (2021). STING regulates metabolic reprogramming in macrophages via HIF-1α during Brucella infection. PLoS Pathog. 17:e1009597. doi: 10.1371/journal.ppat.1009597]. It should be [Costa Franco, M., Marim, F., Guimarães, E., Assis, N., Cerqueira, D., Alves-Silva, J., et al. (2018). Brucella abortus triggers a cGAS-independent STING pathway to induce host protection that involves guanylate-binding proteins and inflammasome activation. J. Immunol. 200, 607-622. doi: 10.4049/jimmunol.1700725;Meunier, E., Wallet, P., Dreier, R., Costanzo, S., Anton, L., Rühl, S., et al. (2015). Guanylate-binding proteins promote activation of the AIM2 inflammasome during infection with Francisella novicida. Nat. Immunol. 16, 476-484. doi: 10.1038/ni.3119]. The original version of this article has been updatedThe reference for [Burdette et al., 2011] was erroneously written as [Burdette, D., Monroe, K., Sotelo-Troha, K., Iwig, J., Eckert, B., Hyodo, M., et al. (2011). STING is a direct innate immune sensor of cyclic di-GMP. Nature 478, 515-518. doi: 10.1038/nature10429]. It should be [Costa Franco, M., Marim, F., Guimarães, E., Assis, N., Cerqueira, D., Alves-Silva, J., et al. (2018). Brucella abortus triggers a cGAS-independent STING pathway to induce host protection that involves guanylate-binding proteins and inflammasome activation. J. Immunol. 200, 607-622. doi: 10.4049/jimmunol.1700725]. The reference for [Meunier et al., 2015;Figure 2] was erroneously written as [Meunier, E., Wallet, P., Dreier, R., Costanzo, S., Anton, L., Rühl, S., et al. (2015). Guanylate-binding proteins promote activation of the AIM2 inflammasome during infection with Francisella novicida. Nat. Immunol. 16, 476-484. doi: 10.1038/ni.3119]. It should be [Chen, Q., Sun, L., and Chen, Z. (2016). Regulation and function of the cGAS-STING pathway of cytosolic DNA sensing. Nat. Immunol. 17, 1142Immunol. 17, -1149Immunol. 17, . doi: 10.1038/ni.3558]/ni.3558]. The reference for [Li et al., 2021] was erroneously written as [Li, R., Liu, W., Yin, X., Zheng, F., Wang, Z., Wu, X., et al. (2021). Brucella spp. Omp25 promotes proteasome-mediated cGAS degradation to attenuate IFN-β production. Front. Microbiol. 12:702881. doi: 10.3389/fmicb.2021.702881]. It should be [Gomes, M., Guimarães, E., Marinho, F., Macedo, I., Aguiar, E., Barber, G., et al. (2021). STING regulates metabolic reprogramming in macrophages via HIF-1α during Brucella infection. PLoS Pathog. 17:e1009597. doi: 10.1371/journal.ppat.1009597]. The reference for [Khan et al., 2020] was erroneously written as [Khan, M., Harms, J., Liu, Y., Eickhoff, J., Tan, J., Hu, T., et al. (2020). Brucella suppress STING expression via miR-24 to enhance infection. PLoS Pathog. 16:e1009020. doi: 10.1371/journal.ppat.1009020]. It should be [Li, R., Liu, W., Yin, X., Zheng, F., Wang, Z., Wu, X., et al. (2021). Brucella spp. Omp25 promotes proteasomemediated cGAS degradation to attenuate IFN-β production. Front. Microbiol. 12:702881. doi: 10.3389/fmicb.2021.702881]. The reference for [Grilló et al., 2012] was erroneously written as [Grilló, M., Blasco, J., Gorvel, J., Moriyón, I., and Moreno, E. (2012). What have we learned from brucellosis in the mouse model? Vet. Res. 43:29. doi: 10.1186Res. 43:29. doi: 10. /1297-9716-43-29]-9716-43-29]. It should be [Khan, M., Harms, J., Liu, Y., Eickhoff, J., Tan, J., Hu, T., et al. (2020). Brucella suppress STING expression via miR-24 to enhance infection. PLoS Pathog. 16:e1009020. doi: 10.1371/journal.ppat.1009020]. The original version of this article has been updatedThe reference for [Wang et al., 2021b] was erroneously written as [Wang, Z., Wang, Y., Yang, H., Guo, J., and Wang, Z. (2021b). Doxycycline induces apoptosis of Brucella suis S2 strain-infected HMC3 microglial cells by activating calreticulindependent JNK/p53 signaling pathway. Front. Cell. Infect. Microbiol. 11:640847. doi: 10.3389/fcimb.2021.640847]. It should be [Grilló, M., Blasco, J., Gorvel, J., Moriyón, I., and Moreno, E. (2012). What have we learned from brucellosis in the mouse model? Vet. Res. 43:29. doi: 10.1186Res. 43:29. doi: 10. /1297-9716-43-29]-9716-43-29]. The original version of this article has been updatedThe reference for [Lee et al., 2014;Wang et al., 2021b] was erroneously written as [Lee, J., Kim, J., Kim, D., Kim, D., Simborio, H., Min, W., et al. (2014). Characterization of betaine aldehyde dehydrogenase (BetB) as an essential virulence factor of Brucella abortus. Vet. Microbiol. 168, 131-140. doi: 10.1016Microbiol. 168, 131-140. doi: 10. /j.vetmic.2013.10. 007;.10. 007;Wang, Z., Wang, Y., Yang, H., Guo, J., and Wang, Z. (2021b). Doxycycline induces apoptosis of Brucella suis S2 strain-infected HMC3 microglial cells by activating calreticulin-dependent JNK/p53 signaling pathway. Front. Cell. Infect. Microbiol. 11:640847. doi: 10.3389/fcimb.2021.640847]. It should be [ Barquero-Calvo, E., Chaves-Olarte, E., Weiss, D., Guzmán-Verri, C., Chacón-Díaz, C., Rucavado, A., et al. (2007). Brucella abortus uses a stealthy strategy to avoid activation of the innate immune system during the onset of infection. PLoS One 2:e631. doi: 10.1371/journal.pone.0000631; Grilló, M., Blasco, J., Gorvel, J., Moriyón, I., and Moreno, E. (2012). What have we learned from brucellosis in the mouse model? Vet. Res. 43:29. doi: 10.1186Res. 43:29. doi: 10. /1297-9716-43-29]-9716-43-29]. The reference for [Lee et al., 2014] was erroneously written as [Lee, J., Kim, J., Kim, D., Kim, D., Simborio, H., Min, W., et al. (2014). Characterization of betaine aldehyde dehydrogenase (BetB) as an essential virulence factor of Brucella abortus. Vet. Microbiol. 168, 131-140. doi: 10.1016Microbiol. 168, 131-140. doi: 10. /j.vetmic.2013.10. 007.10. 007]. It should be [ Barquero-Calvo, E., Chaves-Olarte, E., Weiss, D., Guzmán-Verri, C., Chacón-Díaz, C., Rucavado, A., et al. (2007). Brucella abortus uses a stealthy strategy to avoid activation of the innate immune system during the onset of infection. PLoS One 2:e631. doi: 10.1371/journal.pone.0000631]. The reference for [Wang et al., 2021b] was erroneously written as [Wang, Z., Wang, Y., Yang, H., Guo, J., and Wang, Z. (2021b). Doxycycline induces apoptosis of Brucella suis S2 strain-infected HMC3 microglial cells by activating calreticulindependent JNK/p53 signaling pathway. Front. Cell. Infect. Microbiol. 11:640847. doi: 10.3389/fcimb.2021.640847]. It should be [Grilló, M., Blasco, J., Gorvel, J., Moriyón, I., and Moreno, E. (2012). What have we learned from brucellosis in the mouse model? Vet. Res. 43:29. doi: 10.1186Res. 43:29. doi: 10. /1297-9716-43-29]-9716-43-29]. The reference for [Wang et al., 2021b] was erroneously written as [Wang, Z., Wang, Y., Yang, H., Guo, J., and Wang, Z. (2021b). Doxycycline induces apoptosis of Brucella suis S2 strain-infected HMC3 microglial cells by activating calreticulindependent JNK/p53 signaling pathway. Front. Cell. Infect. Microbiol. 11:640847. doi: 10.3389/fcimb.2021.640847]. It should be [Grilló, M., Blasco, J., Gorvel, J., Moriyón, I., and Moreno, E. (2012). What have we learned from brucellosis in the mouse model? Vet. Res. 43:29. doi: 10.1186Res. 43:29. doi: 10. /1297-9716-43-29]-9716-43-29]. The original version of this article has been updatedThe reference for [Wang et al., 2021b] was erroneously written as [Wang, Z., Wang, Y., Yang, H., Guo, J., and Wang, Z. (2021b). Doxycycline induces apoptosis of Brucella suis S2 strain-infected HMC3 microglial cells by activating calreticulindependent JNK/p53 signaling pathway. Front. Cell. Infect. Microbiol. 11:640847. doi: 10.3389/fcimb.2021.640847]. It should be [Grilló, M., Blasco, J., Gorvel, J., Moriyón, I., and Moreno, E. (2012). What have we learned from brucellosis in the mouse model? Vet. Res. 43:29. doi: 10.1186Res. 43:29. doi: 10. /1297-9716-43-29]-9716-43-29]. The reference for [Starr et al., 2012] was erroneously written as [Starr, T., Child, R., Wehrly, T., Hansen, B., Hwang, S., López-Otin, C., et al. (2012). Selective subversion of autophagy complexes facilitates completion of the Brucella intracellular cycle. Cell Host Microbe 11, 33-45. doi: 10.1016Microbe 11, 33-45. doi: 10. /j.chom.2011.12.002.12.002]. It should be [Guo, X., Zeng, H., Li, M., Xiao, Y., Gu, G., Song, Z., et al. (2023). The mechanism of chronic intracellular infection with Brucella spp. Front. Cell. Infect. Microbiol. 13:1129172. doi: 10.3389/fcimb.2023.1129172]. The reference for [Li C. et al., 2022] was erroneously written as [Li, C., Wang, J., Sun, W., Liu, X., Wang, J., and Peng, Q. (2022). The Brucella effector BspI suppresses inflammation via inhibition of IRE1 kinase activity during Brucella infection. J. Immunol. 209, 488-497. doi: 10.4049/jimmunol.2200001]. It should be [Zhang, G., Hu, H., Yin, Y., Tian, M., Bu, Z., Ding, C., et al. (2024). Brucella manipulates host cell ferroptosis to facilitate its intracellular replication and egress in RAW264.7 macrophages. Antioxidants (Basel) 13:577. doi: 10.3390/antiox13050577]. Missing in-text citation [Wang, Z., Wang, Y., Yang, H., Guo, J., and Wang, Z. (2021b). Doxycycline induces apoptosis of Brucella suis S2 strain-infected HMC3 microglial cells by activating calreticulin-dependent JNK/p53 signaling pathway. Front. Cell. Infect. Microbiol. 11:640847. doi: 10.3389/fcimb.2021.640847] was not cited in the article. The citation has now been inserted in the section [8 Summary and outlook, Paragraph 1] and should read: "[Brucella has co-evolved with its hosts over millions of years, developing a range of virulence strategies that facilitate its survival and ultimately lead to disease onset through the manipulation of host systems. Brucella employs several primary strategies to evade the host immune system, enabling its proliferation and sustained intracellular survival, which leads to chronic infection. These include the following: inhibition of complement and TLR pathways; blockage of maturation and disruption of antigen presentation by DCs; formation of intracellular replication vesicles; and manipulation of autophagy, ER stress, inflammasome activation, pyroptosis, apoptosis, ferroptosis, and the cGAS-STING pathway, among others. Brucella produces virulence factors and effector proteins that manipulate host cell signaling pathways, disrupting normal cellular processes to its advantage. However, the mechanisms by which some effector proteins regulate cellular processes during infection are poorly understood. Autophagy and programed cell death pathways (e.g., pyroptosis, apoptosis, and ferroptosis) serve as host defense strategies, containing infections by eliminating intracellular pathogens from infected cells (Li C. et al., 2022). However, Brucella can exploit programed cell death pathways to evade killing, employing specific molecular mechanisms to enhance its replication, survival, and dissemination within host cells. Therefore, researchers can disrupt the specific molecular mechanisms by which Brucella manipulates autophagy, pyroptosis, apoptosis, and ferroptosis, enabling the corresponding cell death program to proceed as normal and thereby eradicating the bacteria. Doxycycline (Dox) can inhibit CALR protein expression, activate the JNK/p53 signaling pathway, and induce apoptosis in HMC3 cells, thereby achieving the therapeutic goal of treating brucellosis (Wang et al.,2021b). The interaction between Brucella and programed cell death remains unclear. Thus, elucidation of the mechanisms governing these interactions is essential for identifying potential drug targets that could induce programed cell death and eradicate the pathogen.]" The original version of this article has been updated. here, please contact the journal's editorial office.