4.4 Article

Fcγ receptor regulation of Citrobacter rodentium infection

Journal

INFECTION AND IMMUNITY
Volume 76, Issue 4, Pages 1728-1737

Publisher

AMER SOC MICROBIOLOGY
DOI: 10.1128/IAI.01493-07

Keywords

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Funding

  1. NIDDK NIH HHS [R01 DK051362, DK44319, DK51362, R37 DK044319, R01 DK053056, R01 DK53056, R01 DK044319] Funding Source: Medline

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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 immumoglobulin 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 Fc gamma receptors (Fc gamma Rs), the receptors for the Fc portion of IgG, regulate this bacterial infection within mucosal tissues. Therefore, we investigated the roles of Fc gamma Rs during C. rodentium infection. Fe receptor common gamma chain (FcR gamma)-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 Fc gamma Rs, phagocytosis by macrophages was significantly diminished. Therefore, activating Fc gamma Rs 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.

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