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Infect. Immun. doi:10.1128/IAI.01493-07
Copyright (c) 2008, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Fc Receptor Regulation of Citrobacter rodentium Infection

Department of Gastroenterology, Kobe University School of Medicine, Department of Experimental Immunology, Institute of Development, Aging and Cancer, Tohoku University, Japan, Gastroenterology Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, Department of Medical Pharmaceutics, Kobe Pharmaceutical University, Japan

^* To whom correspondence should be addressed. Email: myoshida{at}med.kobe-u.ac.jp.

	Abstract

Citrobacter rodentium (C. rodentium), a murine model pathogen for enteropathogenic E coli, colonizes the colon utilizing attaching and effacement lesions (A/E lesion) to adhere specifically to the surface of intestinal epitherial cells and cause mucosal inflammation. CD4⁺ T cells, B cells and IgG, but not secretory IgA or IgM, play a critical role in eradicating this pathogen. Consistent with the importance of IgG in C. rodentium eradiation, IgG transport by the neonatal Fc receptor for IgG (FcRn) within the intestinal epithelium also has a critical role in the regulation of C. rodentium infection. It remains to be determined, however, whether Fc receptors (R) regulate this bacterial infection within mucosal tissues. Therefore, we investigated the role of FcRs during C. rodentium infection. FcR-chain (FcR) 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 FcR, phagocytosis by macrophages was significantly diminished. Therefore, activating FcRs 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.