Editorial: Mechanisms during bacterial infection: cellular recognition, signalling, and regulation

COPYRIGHT © 2023 Cho and Kim. This is an openaccess 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) and the copyright owner(s) 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. TYPE Editorial PUBLISHED 26 September 2023 DOI 10.3389/fcimb.2023.1286423

specific recognition, binding, interaction, and adhesion, as well as the regulation of host signaling.
Although a variety of cellular adhesion factors that are associated with interactions between pathogens and host cells in epithelial cells have been reported, information on the role of glycan in infections and signaling is limited.Most studies have focused on pathogenic factors-related symptoms in the pathogenesis of bacterial infections.Glycan-based pathogenicity, a lectin-glycan interaction (LGI) concept, has been proposed (Cho et al., 2022).LGIs can be systemically expanded during the immune response by the host glycans in the pathogenesis of infectious diseases (Kim, 2022a;Kim, 2022b).Notably, hosts and bacteria have evolved and use the same machinery, in which bacterial pathogens and hosts reciprocally utilize own proteins and glycans to invade and progress, respectively.
Yang et al. described the effect of coaggregation between two bacteria on human gingival epithelial cells (hGECs).The known subgingival plaque biofilms produced by Fusobacterium nucleatum were involved in the development of periodontitis.Another gingival pathogen, Streptococcus gordonii, coaggregated with periodontal pathogens and colonized the hGECs.Coaggregation between F. nucleatum and S. gordonii synergized subgingival plaque biofilms virulence.Although the coaggregation inhibited F. nucleatum adhesion and invasion into hGECs, it enhanced S. gordonii adhesion to hGECs.Mechanically, coaggregation increased the levels of innate immune receptors of Toll-like receptor (TLR)2 and TLR4 in hGECs.In addition, coaggregation inhibited hGEC apoptosis and promoted the secretion of proinflammatory cytokines tumor necrosis factor (TNF)-a and interleukin (IL)-6 by hGECs through TLR2/TLR4/NF-kB/MAPK signaling.However, coaggregation inhibited the secretion of anti-inflammatory cytokine transforming growth factor (TGF)-b1, to upregulate the p65/p38/ JNK/NF-kB/MAPK signaling axis, and consequently, aggravated the host inflammatory response.Therefore, coaggregation suppressed the adhesion and invasion of F. nucleatum but promoted S. gordonii adhesion to hGECs.
Zhang et al. described Fusobacterium necrophorum, a pathogenic inducer of bovine foot rot characterized by a strong inflammatory response.Using a cow skin explant model, the authors reported that F. necrophorum bacillus induced inflammation with tissue cell apoptosis.F. necrophorum infection upregulated p-IkBa and nuclear factor (NF)-kB p65 levels via the NF-kB p65/TNF-a/IL-1b/IL-8 pathway, inducing an inflammatory response, and causing foot rot in dairy cows.
Singh et al. described membrane phospholipase-C (PLC) as a determinant of host-pathogen interaction in bacterial infections and bacterial infections pathogenesis in humans.Virulence factors are also associated with pathogenic bacteria survival, proliferation, and colonization in the host.Apart from protein interactions, the authors also identified PLC, an enzyme virulence factor, as a cell signaling and regulatory factor.PLC catalytically hydrolyzes membrane phospholipid to di-acyl-glycerol and inositol triphosphate.The products act as secondary messengers to activate signaling involved in the immune response.The involvement of PLCs in infectious diseases has not been well explained to date, although both the host and pathogen PLCs are directly linked to infections, pathogenesis, and disease symptoms.
The authors systemically reviewed the pathogenic determinant PLC in infections, host recognition, and pathogenesis.Jia et al. described Porphyromonas gingivalis-caused insulin resistance and its signaling.The Porphyromonas gingivalis (P.gingivalis), a gram-negative oral anaerobic bacteria, produced multiple toxins which contributed to periodontal pathogenesis and systemic diseases.The virulence factors disturbed the host's innate and adaptive immunities to evade the host's immune surveillance.In their study, for insulin resistance caused by P. gingivalis, bacteria-induced systemic inflammation disturbed insulin signaling through dysfunctional pancreatic b-cells and lowered insulin sensitivity-based insulin resistance.The authors presented a systematic overview and discussed the literature on P. gingivalis-driven insulin resistance and the relationship between insulin resistance as a systemic disease and P. gingivalis infection.Then, therapeutic approaches were proposed with insight into the current research directions and systemic disease-blocking.
In summary, the two original articles and two reviews present the latest information and most recent research results on bacterial and cellular recognition, signaling, and the regulation of innate immune aspects.Bacterial/host innate immunity is an immunological defense that involves binding on certain functional target molecules, such as glycans, proteins, and enzymes.The target molecules are directly associated with human diseases and also act against pathogenic invaders and self-associated patterns.This review provides an overview of basic innate immunity and the mechanisms of pathogenic bacteria and host cell interactions during infections and the inflammatory response.The articles that were reviewed were studies on pathogenic bacteria signaling and therapeutic approaches.This Topic provides insight into the emerging effector molecules associated with pathogenic adhesion to host cells and relevant treatment strategies for infectious diseases.

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