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Fcgamma receptor regulation of Citrobacter rodentium infection.

Authors :
Masuda A
Yoshida M
Shiomi H
Ikezawa S
Takagawa T
Tanaka H
Chinzei R
Ishida T
Morita Y
Kutsumi H
Inokuchi H
Wang S
Kobayashi K
Mizuno S
Nakamura A
Takai T
Blumberg RS
Azuma T
Source :
Infection and immunity [Infect Immun] 2008 Apr; Vol. 76 (4), pp. 1728-37. Date of Electronic Publication: 2008 Jan 28.
Publication Year :
2008

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

Details

Language :
English
ISSN :
1098-5522
Volume :
76
Issue :
4
Database :
MEDLINE
Journal :
Infection and immunity
Publication Type :
Academic Journal
Accession number :
18227164
Full Text :
https://doi.org/10.1128/IAI.01493-07