10.17169/REFUBIUM-27837
Heimesaat, Markus M.
Genger, Claudia
Biesemeier, Nina
Klove, Sigri
Weschka, Dennis
Mousavi, Soraya
Bereswill, Stefan
Inflammatory Immune Responses and Gut Microbiota Changes Following Campylobacter coli Infection of IL-10 -/- Mice with Chronic Colitis
Charité - Universitätsmedizin Berlin
2020
Campylobacter coli
murine chronic colitis
host-pathogen interaction
aged IL-10-/- mice
intestinal immunopathology
bacterial colonization
gut microbiota changes
dysbiosis
enterobacterial overgrowth
intestinal and systemic immune responses
600 Technik, Medizin, angewandte Wissenschaften::610 Medizin und Gesundheit::610 Medizin und Gesundheit
Universitätsbibliothek der FU Berlin
Universitätsbibliothek der FU Berlin
2020-09-11
2020-09-11
2020
Wissenschaftlicher Artikel
https://refubium.fu-berlin.de/handle/fub188/28087
10.3390/pathogens9070560
32664563
Human infections with the food-borne enteropathogens Campylobacter are progressively rising. Recent evidence revealed that pre-existing intestinal inflammation facilitates enteropathogenic infection subsequently exacerbating the underlying disease. Given that only little is known about C. coli-host interactions and particularly during intestinal inflammation, the aim of the present study was to survey gastrointestinal colonization properties, gut microbiota changes and pro-inflammatory sequelae upon peroral C. coli-infection of IL-10-/- mice with chronic colitis. C. coli colonized the gastrointestinal tract of mice with varying efficiencies until day 28 post-infection and induced macroscopic and microscopic inflammatory changes as indicated by shorter colonic lengths, more distinct histopathological changes in the colonic mucosa and higher numbers of apoptotic colonic epithelial cells when compared to mock-infected controls. Furthermore, not only colonic innate and adaptive immune cell responses, but also enhanced systemic TNF-α secretion could be observed following C. coli as opposed to mock challenge. Notably, C. coli induced intestinal inflammatory sequelae were accompanied with gut microbiota shifts towards higher commensal enterobacterial loads in the infected gut lumen. Moreover, the pathogen translocated from the intestinal tract to extra-intestinal tissue sites in some cases, but never to systemic compartments. Hence, C. coli accelerates inflammatory immune responses in IL-10-/- mice with chronic colitis.