Journal
MUCOSAL IMMUNOLOGY
Volume 6, Issue 1, Pages 177-188Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/mi.2012.61
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Funding
- Deutsche Forschungsgemeinschaft (D. F. G.) [Ni575/6-2, Ni575/7-1]
- Zukunftspreis from German Association for the Study of Inflammatory Bowel Disease (DACED)
- International Graduate School of Molecular Medicine of Ulm University [GSC270]
- summer school Host-Microbe Interactions in the Intestinal Tract Kiel, Germany
- German Gastroenterology Society (DGVS)
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Innate immune cells, such as intestinal epithelial cells, dendritic cells (DCs), macrophages, granulocytes, and innate lymphoid cells provide a first line of defence to enteric pathogens. To study the role of CX(3)CR1(+) DCs and macrophages in host defence, we infected CX(3)CR1-GFP animals with Citrobacter rodentium. When transgenic CX(3)CR1-GFP animals are infected with the natural mouse pathogen C. rodentium, CX(3)CR1(-/-) animals showed a delayed clearance of C. rodentium as compared with (age- and sex-matched) wild-type B6 animals. The delayed clearance of C. rodentium is associated with reduced interleukin (IL)-22 expression. In C. rodentium-infected CX(3)CR1-GFP animals, IL-22 producing lymphoid-tissue inducer cells (LTi cells) were selectively reduced in the absence of CX(3)CR1. The reduced IL-22 expression correlates with decreased expression of the antimicrobial peptides RegIII beta and RegIII gamma The depletion of CX(3)CR1(+) cells by diphtheria toxin injection in CX(3)CR1-GFPxCD11c.DOG animals confirmed the role of CX(3)CR1(+) phagocytes in establishing IL-22 production, supporting the clearance of a C. rodentium infection.
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