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.