Abstract
An acute and persistent eosinophil infiltration is observed during Mycobacterium bovis BCG pleural infection in mice. Eosinophil accumulation, lipid body formation, and eotaxin production were significantly reduced in BCG-infected Toll-like receptor-2 (TLR2)-deficient mice compared to wild-type mice. Neutralization of eotaxin or CCR3 drastically inhibited BCG-induced eosinophil accumulation and lipid body formation, indicating that BCG-induced eosinophil recruitment and activation is largely dependent of TLR2-mediated eotaxin generation.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Chemokine CCL11
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Chemokines, CC / physiology*
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Chemotactic Factors, Eosinophil / physiology*
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Chemotaxis, Leukocyte / immunology*
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Eosinophils / cytology
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Eosinophils / immunology*
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Eosinophils / metabolism
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Mice
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Mice, Inbred C57BL
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Mice, Knockout
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Mycobacterium bovis / immunology*
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Receptors, CCR3
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Receptors, Chemokine / physiology*
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Toll-Like Receptor 2 / deficiency
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Toll-Like Receptor 2 / genetics
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Toll-Like Receptor 2 / physiology*
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Tuberculosis, Pleural / immunology*
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Tuberculosis, Pleural / metabolism
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Tuberculosis, Pleural / veterinary
Substances
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Ccl11 protein, mouse
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Ccr3 protein, mouse
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Chemokine CCL11
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Chemokines, CC
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Chemotactic Factors, Eosinophil
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Receptors, CCR3
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Receptors, Chemokine
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Tlr2 protein, mouse
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Toll-Like Receptor 2