期刊
JOURNAL OF IMMUNOLOGY
卷 168, 期 3, 页码 1447-1456出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.168.3.1447
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The role of CXCR during allergic airway and asthmatic diseases is yet to be fully characterized. Therefore, the present study addressed the role of CXCR2 during Aspergillus fundigatus-induced asthma. Mice deficient in CXCR2 (CXCR2(-/-)) and wild-type counterparts (CXCR2(+/+)) were sensitized toA.fumigatus Ags and challenged with A.fumigatus conidia, and the resulting allergic airway disease was monitored for up to 37 days. At days 3 and 7 after conidia, CXCR2(-/-) mice exhibited significantly greater methacholine-induced airway hyperreactivity than did CXCR2(+/+) mice. In contrast, CXCR2-deficient mice exhibited significantly less airway hyperresponsiveness than the wild-type control groups at days 14 and 37 after conidia. At all times after conidia, whole lung levels of IL-4, IL-5, and eotaxin/CC chemokine ligand 11 were significantly lower in CXCR2(-/-) mice than in the wild-type controls. Eosinophil and T cell, but not neutrophil, recruitment into the airways of A. fumigatus-sensitized CXCR2(-/-) mice was significantly impaired compared with wild-type controls at all times after the conidia challenge. Whole lung levels of IFN-gamma, inflammatory protein-10/CXC ligand (CXCL) 10, and monokine induced by IFN-gamma (MIG)/CXCL9 were significantly increased in CXCR2(-/-) mice compared with CXCR2(+/+) mice at various times after conidia. Interestingly, at day 3 after conidia, neutrophil recruitment and airway hyperresponsiveness in CXCR2(-/-) mice was mediated by inflammatory protein-10/CXCL10 and, to a lesser degree, MIG/CXCL9. Taken together, these data suggest that CXCR2 contributes to the persistence of asthmatic disease due to A. fumigatus.
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