Abstract

BackgroundCD163 is one of the scavenger receptors that are specifically expressed on macrophages and are well known to be upregulated by various inflammatory responses, including chronic obstructive pulmonary disease in airway diseases. ObjectiveTo evaluate the CD163 expression in the lungs of patients with fatal asthma and investigated whether CD163 contributes to the pathogenesis in asthma. MethodsThe CD163 expressions in the lungs of patients with fatal asthma (n = 9) and in those of nonasthma control subjects (n = 8) were tested by immunohistochemistry. In mouse models of asthma, airway hyperresponsiveness (AHR) and the numbers of airway inflammatory cells in the bronchoalveolar lavage fluid (BALF) were analyzed in the CD163-deficient mice and the control wild-type mice. ResultsThe numbers of CD163-positive macrophages in the lung tissues were significantly increased in the all 6 patients with fatal asthma than in the control subjects. In mouse models of asthma, AHR and the numbers of infiltrating leukocytes, such as eosinophils, lymphocytes, neutrophils, and macrophages, in the BALF were significantly decreased in the CD163-deficient mice when compared with control wild-type mice. The concentrations of interferon γ and interleukin 5 in the BALF were significantly decreased in the CD163-deficient mice when compared with those in the control wild-type mice. ConclusionCD163 may play important roles in airway inflammation and AHR in asthma.

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