Chlamydia trachomatis pulmonary infection induces greater inflammatory pathology in immunoglobulin A deficient mice

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.