| First Author | Jing X | Year | 2020 |
| Journal | Front Immunol | Volume | 11 |
| Pages | 579615 | PubMed ID | 33488580 |
| Mgi Jnum | J:335336 | Mgi Id | MGI:6729313 |
| Doi | 10.3389/fimmu.2020.579615 | Citation | Jing X, et al. (2020) IL-23 Contributes to Campylobacter jejuni-Induced Intestinal Pathology via Promoting IL-17 and IFNgamma Responses by Innate Lymphoid Cells. Front Immunol 11:579615 |
| abstractText | Human pathogen Campylobacter jejuni is a significant risk factor for the development of long-term intestinal dysfunction although the cellular and molecular mechanisms remain scantily defined. IL-23 is an emerging therapeutic target for the treatment of inflammatory intestinal diseases, however its role in C. jejuni-driven intestinal pathology is not fully understood. IL-10 deficient mice represent a robust model to study the pathogenesis of C. jejuni infection because C. jejuni infection of mice lacking IL-10 results in symptoms and pathology that resemble human campylobacteriosis. To determine the role of IL-23 in C. jejuni-driven intestinal inflammation, we studied the disease pathogenesis in IL-23(-/-) mice with inhibited IL-10Ralpha signaling. These mice exhibited reduced intestinal pathology independent from bacterial clearance. Further, levels of IFNgamma, IL-17, IL-22, TNF, and IL-6 were reduced and associated with reduced accumulation of neutrophils, monocytes and macrophages in the colon. Flow cytometry analysis revealed reduced production of IL-17 and IFNgamma by group 1 and 3 innate lymphoid cells. Thus, our data suggest that IL-23 contributes to intestinal inflammation in C. jejuni infected mice by promoting IL-17 and IFNgamma production by innate lymphoid cells. |
