Abstract
IL-10 regulates the balance of an immune response between pathogen clearance and immunopathology. We show here that Mycobacterium tuberculosis (Mtb) infection in the absence of IL-10 (IL-10(-/-) mice) results in reduced bacterial loads in the lung. This reduction was preceded by an accelerated and enhanced IFN-γ response in the lung, an increased influx of CD4(+) T cells into the lung, and enhanced production of chemokines and cytokines, including CXCL10 and IL-17, in both the lung and the serum. Neutralization of IL-17 affected neither the enhanced production of CXCL10 nor the accumulation of IFN-γ-producing T cells in the lungs, but led to reduced numbers of granulocytes in the lung and reduced bacterial loads in the spleens of Mtb-infected mice. This suggests that IL-17 may contribute to dissemination of Mtb.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Antibodies, Blocking / pharmacology
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Bacterial Load / drug effects
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Bacterial Load / genetics
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Bacterial Load / immunology
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CD4-Positive T-Lymphocytes / drug effects
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CD4-Positive T-Lymphocytes / immunology
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CD4-Positive T-Lymphocytes / metabolism*
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CD4-Positive T-Lymphocytes / microbiology
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CD4-Positive T-Lymphocytes / pathology
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Cell Movement
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Cells, Cultured
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Chemokine CXCL10 / biosynthesis
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Chemokine CXCL10 / genetics
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Female
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Interferon-gamma / biosynthesis*
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Interferon-gamma / genetics
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Interleukin-10 / genetics
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Interleukin-17 / biosynthesis*
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Interleukin-17 / genetics
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Interleukin-17 / immunology
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Lung / immunology
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Lung / metabolism*
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Lung / microbiology
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Lung / pathology
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Mice
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Mice, Inbred BALB C
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Mice, Inbred C57BL
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Mice, Knockout
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Mycobacterium tuberculosis / immunology*
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Mycobacterium tuberculosis / pathogenicity
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Th1-Th2 Balance / drug effects
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Tuberculosis / genetics
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Tuberculosis / immunology*
Substances
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Antibodies, Blocking
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Chemokine CXCL10
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Interleukin-17
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Interleukin-10
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Interferon-gamma