期刊
MUCOSAL IMMUNOLOGY
卷 14, 期 4, 页码 923-936出版社
ELSEVIER SCIENCE INC
DOI: 10.1038/s41385-021-00386-7
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资金
- Projekt DEAL
IL-33 signaling pathway plays a critical role in regulating the immune response to enteric pathogens, affecting the colitis caused by microbial invasion. Deficiency of IL-33 can attenuate bacterial-induced colitis, while boosting its pathway can exacerbate the inflammatory response.
A wide range of microbial pathogens is capable of entering the gastrointestinal tract, causing infectious diarrhea and colitis. A finely tuned balance between different cytokines is necessary to eradicate the microbial threat and to avoid infection complications. The current study identified IL-33 as a critical regulator of the immune response to the enteric pathogen Citrobacter rodentium. We observed that deficiency of the IL-33 signaling pathway attenuates bacterial-induced colitis. Conversely, boosting this pathway strongly aggravates the inflammatory response and makes the mice prone to systemic infection. Mechanistically, IL-33 mediates its detrimental effect by enhancing gut permeability and by limiting the induction of protective T helper 17 cells at the site of infection, thus impairing host defense mechanisms against the enteric pathogen. Importantly, IL-33-treated infected mice supplemented with IL-17A are able to resist the otherwise strong systemic spreading of the pathogen. These findings reveal a novel IL-33/IL-17A crosstalk that controls the pathogenesis of Citrobacter rodentium-driven infectious colitis. Manipulating the dynamics of cytokines may offer new therapeutic strategies to treat specific intestinal infections.
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