Abstract
Abstract C. difficile colonization and toxin production can lead to a wide range of symptoms from diarrhea to pseudomembranous colitis, systemic disease and death. The host immune status plays an important role in protection against C. difficile infection (CDI), especially the dendritic cells (DCs) as a bridge to connect innate and adaptive immunity. However, their role during CDI has not been characterized. In this study, we adopted a murine model of transgenic mice Tg-CD11c-DTR/EGFP (Tg), whose DCs can be conditionally depleted by injection of diphtheria toxin (DT), to investigate the role of DCs in CDI. We found that DT-injected Tg mice were more vulnerable to the CDI, compared with the PBS-injected Tg mice. DT-injection significantly depleted DCs, impaired the host capability to clear off C. difficile in the intestine, and increased the infiltration of other bacteria into organs. DC deletion did not seem to affect intestinal microbiota, nor neutrophil infiltration into lumen, but reduced macrophage infiltration into intestinal lumen. Interestingly, DC depletion impaired the intestinal barrier integrity, which could partially contribute to the increased infiltration of intestinal bacteria to organs, and severity of CDI. Transferring DCs to wild-type mice conferred host resistance to CDI. These data clearly demonstrate a protective role of DCs against CDI.
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