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Fcγ Receptor Regulation of Citrobacter rodentium Infection▿

By Atsuhiro Masuda, Masaru Yoshida, Hideyuki Shiomi, Satoshi Ikezawa, Tetsuya Takagawa, Hiroshi Tanaka, Ryo Chinzei, Tsukasa Ishida, Yoshinori Morita, Hiromu Kutsumi, Hideto Inokuchi, Shuo Wang, Kanna Kobayashi, Shigeto Mizuno, Akira Nakamura, Toshiyuki Takai, Richard S. Blumberg and Takeshi Azuma

Abstract

Citrobacter rodentium, a murine model pathogen for enteropathogenic Escherichia coli, colonizes the colon utilizing attaching and effacing lesions to adhere specifically to the surfaces of intestinal epithelial cells and cause mucosal inflammation. CD4+ T cells, B cells, and immunoglobulin G (IgG), but not secretory IgA or IgM, play a critical role in eradicating this pathogen. Consistent with the importance of IgG in C. rodentium eradication, IgG transport by the neonatal Fc receptor for IgG within the intestinal epithelium also has a critical role in the regulation of C. rodentium infection. It remains to be determined, however, whether Fcγ receptors (FcγRs), the receptors for the Fc portion of IgG, regulate this bacterial infection within mucosal tissues. Therefore, we investigated the roles of FcγRs during C. rodentium infection. Fc receptor common gamma chain (FcRγ)-deficient mice were more susceptible to C. rodentium-induced colitis. This occurred through decreased efficiency of FcR-mediated endocytosis and maturation of dendritic cells and consequently T-cell activation of antigen-specific T cells. Moreover, in the absence of FcγRs, phagocytosis by macrophages was significantly diminished. Therefore, activating FcγRs play an important role in defending against C. rodentium infection, indicating that the critical role played by IgG in this infection is not mediated by IgG alone but is dependent upon this class of receptors

Topics: Host Response and Inflammation
Publisher: American Society for Microbiology (ASM)
OAI identifier: oai:pubmedcentral.nih.gov:2292883
Provided by: PubMed Central
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