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Interleukin-22 regulates the complement system to promote resistance against pathobionts after pathogen-induced intestinal damage.


ABSTRACT: Pathobionts play a critical role in disease development, but the immune mechanisms against pathobionts remain poorly understood. Here, we report a critical role for interleukin-22 (IL-22) in systemic protection against bacterial pathobionts that translocate into the circulation after infection with the pathogen Clostridium difficile. Infection with C. difficile induced IL-22, and infected Il22(-/-) mice harbored high numbers of pathobionts in extraintestinal organs despite comparable pathogen load and intestinal damage in mutant and wild-type mice. Pathobionts exhibited increased resistant against complement-mediated phagocytosis, and their intravenous administration resulted in high animal mortality. Selective removal of translocated commensals rescued Il22(-/-) mice, and IL-22 administration enhanced the elimination of pathobionts. Mechanistically, IL-22 augmented bacterial phagocytosis by increasing the expression and bacterial binding of complement C3. Our study demonstrates an unexpected role for IL-22 in controlling the elimination of pathobionts that enter the systemic circulation through the regulation of the complement system.

SUBMITTER: Hasegawa M 

PROVIDER: S-EPMC4220303 | biostudies-literature | 2014 Oct

REPOSITORIES: biostudies-literature

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Interleukin-22 regulates the complement system to promote resistance against pathobionts after pathogen-induced intestinal damage.

Hasegawa Mizuho M   Yada Shoko S   Liu Meng Zhen MZ   Kamada Nobuhiko N   Muñoz-Planillo Raúl R   Do Nhu N   Núñez Gabriel G   Inohara Naohiro N  

Immunity 20141001 4


Pathobionts play a critical role in disease development, but the immune mechanisms against pathobionts remain poorly understood. Here, we report a critical role for interleukin-22 (IL-22) in systemic protection against bacterial pathobionts that translocate into the circulation after infection with the pathogen Clostridium difficile. Infection with C. difficile induced IL-22, and infected Il22(-/-) mice harbored high numbers of pathobionts in extraintestinal organs despite comparable pathogen lo  ...[more]

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