Chlamydia trachomatis is an intracellular bacterial pathogen that primarily infects via mucosal surfaces. Using mice with a targeted disruption in IgA gene expression (IgA -/- mice), we have studied the contribution of IgA, the principal mucosal antibody isotype, in primary immune defenses against pulmonary C. trachomatis infection. Bacterial burden was comparable between IgA -/- and IgA +/+ animals following C. trachomatis challenge. Serum and pulmonary anti-Chlamydia antibody levels were higher in IgA -/- animals, with the exception of IgA. Lung sections of challenged IgA -/- mice showed more extensive immunopathology than corresponding IgA +/+ animals. Real-time PCR analysis demonstrated significantly greater IFN-γ and TGF-β mRNA expression in IgA -/- as compared to IgA +/+ animals. Together, these results suggest that IgA may not be necessary for clearance of primary C. trachomatis infection. However, IgA -/- mice displayed exaggerated lung histopathology and altered cytokine production, indicating an important role for IgA in regulating C. trachomatis induced pulmonary inflammation and maintenance of mucosal homeostasis.
|Idioma original||English (US)|
|Número de páginas||9|
|Estado||Published - jul 2004|
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