Interleukin-33 signaling exacerbates experimental infectious colitis by enhancing gut permeability and inhibiting protective Th17 immunity.

Palmieri, Vittoria; Ebel, Jana-Fabienne; Ngo Thi Phuong, Nhi; Klopfleisch, Robert; Vu, Vivian Pham; Adamczyk, Alexandra; Zöller, Julia; Riedel, Christian; Buer, Jan; Krebs, Philippe; Hansen, Wiebke; Pastille, Eva; Westendorf, Astrid M. (2021). Interleukin-33 signaling exacerbates experimental infectious colitis by enhancing gut permeability and inhibiting protective Th17 immunity. (In Press). Mucosal immunology Springer Nature 10.1038/s41385-021-00386-7

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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.

Item Type:

Journal Article (Original Article)

Division/Institute:

04 Faculty of Medicine > Service Sector > Institute of Pathology > Immunopathology

Graduate School:

Graduate School for Cellular and Biomedical Sciences (GCB)

UniBE Contributor:

Vu, Vivian Pham and Krebs, Philippe

Subjects:

500 Science > 570 Life sciences; biology

ISSN:

1935-3456

Publisher:

Springer Nature

Language:

English

Submitter:

Philippe Krebs

Date Deposited:

11 Mar 2021 09:04

Last Modified:

11 Mar 2021 09:04

Publisher DOI:

10.1038/s41385-021-00386-7

PubMed ID:

33654214

BORIS DOI:

10.48350/153359

URI:

https://boris.unibe.ch/id/eprint/153359

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