Endogenous IL-17 as a factor determining the severity of Clostridium difficile infection in mice
Autor: | Tsutomu Saji, Yoshikazu Ishii, Nobuaki Mori, Yoshikiyo Akasaka, Tomoaki Nakagawa, Chiaki Kajiwara, Soichiro Kimura, Kazuhiro Tateda |
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Rok vydání: | 2016 |
Předmět: |
0301 basic medicine
Microbiology (medical) Diarrhea Chemokine genetic structures Neutrophils medicine.medical_treatment Clostridium difficile toxin A Clostridium difficile toxin B Microbiology Severity of Illness Index 03 medical and health sciences 0302 clinical medicine Intestinal mucosa Cell Movement medicine Animals Intestine Large Enterocolitis Pseudomembranous Mice Knockout Mice Inbred BALB C biology Clostridioides difficile Weight change Body Weight Interleukin-17 General Medicine Clostridium difficile Survival Analysis Disease Models Animal 030104 developmental biology Cytokine Immunology biology.protein Interleukin 17 030215 immunology |
Zdroj: | Journal of medical microbiology. 65(8) |
ISSN: | 1473-5644 |
Popis: | Clostridium difficile infection (CDI) is a toxin-mediated intestinal disease. Toxin A, toxin B and binary toxin are believed to be responsible for the pathogenesis of CDI, which is characterized by massive infiltration of neutrophils at the infected intestinal mucosa. IL-17 is one of the cytokines that play critical roles in several inflammatory and immunological diseases through various actions, including promoting neutrophil recruitment. The aim of this study was to examine the role of this cytokine in CDI by employing IL-17 A and F double knockout (IL-17 KO) mice for the CDI model. We demonstrated that IL-17 KO mice were more resistant to CDI than WT mice using several factors, such as diarrhoea score, weight change and survival rate. Although the bacterial numbers of C. difficile in faeces were not different, the inflammatory mediator levels at the large intestine on day 3 post-infection were attenuated in IL-17 KO mice. Finally, we showed that infiltration of neutrophils, but not macrophages, in the large intestine was significantly decreased in IL-17 KO mice compared to WT mice. In conclusion, the data demonstrate that endogenous IL-17 may be a factor determining the severity of CDI in mice. Although the mechanism is totally unknown, IL-17-mediated inflammatory responses, such as cytokine/chemokine production and neutrophil accumulation, may be plausible targets for future investigations. |
Databáze: | OpenAIRE |
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