期刊
CELLULAR IMMUNOLOGY
卷 230, 期 1, 页码 56-64出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.cellimm.2004.09.002
关键词
Chlamydia trachomatis; immunoglobulin A; inflammation; innate
资金
- NIAMS NIH HHS [AR048973-02] Funding Source: Medline
- NIGMS NIH HHS [S06GM008194-24] Funding Source: Medline
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-gamma and TGF-beta 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. (C) 2004 Elsevier Inc. All rights reserved.
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