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Inhibition of CD163 Signaling Suppress Airway Hyperresponsiveness in Mouse Models of Asthma
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A1321 - Inhibition of CD163 Signaling Suppress Airway Hyperresponsiveness in Mouse Models of Asthma
Author Block: Y. Tokunaga1, H. Imaoka1, Y. Morimatsu1, Y. Kaku1, Y. Sakazaki1, M. Matsuoka1, Y. Fujiwara2, Y. Komohara2, T. Kawayama1, M. Takeya2, T. Hoshino1; 1Department of Medicine, Division of Respirology, Neurology, and Rheumatology, Kurume University School of Medicine, Kurume, Japan, 2Department of Cell Pathology, Graduate School of Medical Sciences, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.
The CD163, a scavenger receptor expressed on macrophages, is known as M2 macrophages marker. M1 and M2 macrophages represent pro- and anti-inflammatory populations, respectively. We reported that CD163 expressed on alveolar macrophages in the lungs of patients with COPD. However, the roles of M2 macrophages in asthma remain unclear. In this study, we investigate the roles of CD163 positive macrophages in lungs of fatal asthma and mouse models of asthma. We used immunohistochemical techniques to examine CD163 expressed on macrophages in the lungs of patients with asthma death (n=7) and nonasthma controls (n=7). The numbers of CD163 positive macrophages in the lung tissues were significantly increased in asthma death patients than control subjects. In mouse models of asthma, airway hyperresponsiveness (AHR) and numbers of eosinophils in the bronchoalveolar lavage fluid (BALF) were significantly decreased in ovalbmin(OVA)-sensitized and challenged CD163 deficient mice, when compared with control wild type mice. Inhibition of CD 163 signaling can be a new treatment target of asthma.
Author Block: Y. Tokunaga1, H. Imaoka1, Y. Morimatsu1, Y. Kaku1, Y. Sakazaki1, M. Matsuoka1, Y. Fujiwara2, Y. Komohara2, T. Kawayama1, M. Takeya2, T. Hoshino1; 1Department of Medicine, Division of Respirology, Neurology, and Rheumatology, Kurume University School of Medicine, Kurume, Japan, 2Department of Cell Pathology, Graduate School of Medical Sciences, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.
The CD163, a scavenger receptor expressed on macrophages, is known as M2 macrophages marker. M1 and M2 macrophages represent pro- and anti-inflammatory populations, respectively. We reported that CD163 expressed on alveolar macrophages in the lungs of patients with COPD. However, the roles of M2 macrophages in asthma remain unclear. In this study, we investigate the roles of CD163 positive macrophages in lungs of fatal asthma and mouse models of asthma. We used immunohistochemical techniques to examine CD163 expressed on macrophages in the lungs of patients with asthma death (n=7) and nonasthma controls (n=7). The numbers of CD163 positive macrophages in the lung tissues were significantly increased in asthma death patients than control subjects. In mouse models of asthma, airway hyperresponsiveness (AHR) and numbers of eosinophils in the bronchoalveolar lavage fluid (BALF) were significantly decreased in ovalbmin(OVA)-sensitized and challenged CD163 deficient mice, when compared with control wild type mice. Inhibition of CD 163 signaling can be a new treatment target of asthma.
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