ORIGINAL RESEARCH article
Front. Immunol.
Sec. Molecular Innate Immunity
Volume 16 - 2025 | doi: 10.3389/fimmu.2025.1556392
Transcriptional responses in different mouse models of septic liver injury differ from those in patients with septic liver injury
Provisionally accepted
- The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, China
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Sepsis, particularly septic liver injury (SLI), is associated with high patient mortality because of its rapid onset and severity. Given the limited availability of human samples, mouse models are commonly utilized to study the pathogenesis of human diseases; however, there is controversy over how well these models mimic the pathophysiological features of SLI in humans. In this study, we evaluated the transcriptomic profiles of human SLI and found that the disease primarily affects progression through the regulation of apoptosis, inflammatory response, nuclear factor kappa-B (NF-κB) and interleukin 17(IL-17) signaling pathways. Subsequently, we analyzed the transcriptomic profiles of two mouse models of SLI and found that both models exhibited an inflammatory response. Furthermore, compared with the lipopolysaccharide (LPS) intraperitoneal injection model, the cecal ligation and puncture (CLP) model recapitulated the phenotype of human septic injury through regulation of neutrophil chemotaxis, apoptosis, and IL-17 signaling, while the LPS model recapitulated the phenotype through immune processes, chemotaxis, and regulation of phagocytosis. Finally, we established the two disease models and validated the expression of differentially expressed genes (DEGs) that are homologs of human genes; only suppressors of cytokine signaling 3 (SOCS3) expression was consistent with the expected trend. Additionally, we analyzed SOCS3 expression levels in sepsis patients at various time intervals, suggesting that SOCS3 reflects the extent of disease progression. In conclusion, our study revealed differences between mouse models and human septic disease. Therefore, the limitations of disease models should be considered when screening for biomarkers and exploring pathogenic mechanisms.
Keywords: SLI, Cecal ligation model, lipopolysaccharide, Immune infiltration, socs3, Microarray
Received: 06 Jan 2025; Accepted: 10 Jul 2025.
Copyright: © 2025 Yan, Fan, He, Zheng and Zhong. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Xiaolin Zhong, The Affiliated Hospital of Southwest Medical University, Luzhou, 646000, Sichuan, China
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