Immune complex-dependent remodeling of the airway vasculature in response to a chronic bacterial infection
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作者:
Aurora, AB
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机构:Univ Calif San Francisco, Dept Microbiol & Immunol, San Francisco, CA 94143 USA
Aurora, AB
Baluk, P
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机构:Univ Calif San Francisco, Dept Microbiol & Immunol, San Francisco, CA 94143 USA
Baluk, P
Zhang, DJ
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机构:Univ Calif San Francisco, Dept Microbiol & Immunol, San Francisco, CA 94143 USA
Zhang, DJ
Sidhu, SS
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机构:Univ Calif San Francisco, Dept Microbiol & Immunol, San Francisco, CA 94143 USA
Sidhu, SS
Dolganov, GM
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机构:Univ Calif San Francisco, Dept Microbiol & Immunol, San Francisco, CA 94143 USA
Dolganov, GM
Basbaum, C
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机构:Univ Calif San Francisco, Dept Microbiol & Immunol, San Francisco, CA 94143 USA
Basbaum, C
McDonald, DM
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机构:Univ Calif San Francisco, Dept Microbiol & Immunol, San Francisco, CA 94143 USA
McDonald, DM
Killeen, N
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Univ Calif San Francisco, Dept Microbiol & Immunol, San Francisco, CA 94143 USAUniv Calif San Francisco, Dept Microbiol & Immunol, San Francisco, CA 94143 USA
Killeen, N
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机构:
[1] Univ Calif San Francisco, Dept Microbiol & Immunol, San Francisco, CA 94143 USA
[2] Univ Calif San Francisco, Dept Anat, San Francisco, CA 94143 USA
[3] Univ Calif San Francisco, Cardiovasc Res Inst, San Francisco, CA 94143 USA
[4] Univ Calif San Francisco, Div Pulm & Crit Care Med, Dept Med, San Francisco, CA 94143 USA
Chronic inflammation in the airways is associated with drama tic architectural changes in the walls of the airways and in thevasculature they contain. In this study, we show that the adaptive immune system is essential for airway remodeling that occurs in mice that are chronically infected with the respiratory pathogen Mycoplasnia pulmonis. Angiogenesis, lymphangiogenesis, and epithelial remodeling were greatly reduced in mice that lacked B cells. Substantiating a role for Ab and airway immune complexes, we found that the transfer of immune serum to B cell-deficient mice could reconstitute pathogen-induced angiogenesis. Inflammatory cells recruited to the infected airways were activated by the humoral response, and this activation correlated with the induction of genes for remodeling factors such as vascular endothelial growth factor-D. The results reveal a novel pathway whereby T cell-dependent Immoral immunity to a persistent airway infection can induce inflammation-dependent angiogenesis, dlymphangiogenesis, and chronic airway pathology.