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• W2912591195 abstract "We have reported that muscarinic M3 receptor antagonist (tiotropium) inhibits the allergic airway inflammation in murine model of asthma. However, the mechanism is still unclear. The purpose of this study is to investigate the effect of muscarinic M3 receptor blockage in development of M2 macrophages in allergic inflammation. Balb/c mice were sensitized and challenged with OVA to develop the mouse model of asthma. During the challenge phase, mice were treated with/without tiotropium. Twenty-four hours after the last challenge, lung cells were isolated from the lung. The lung cells were gated by CD68 positive cells, and analyzed the expression of Relm-α and Arginase-1 (M2 macrophage markers) by flow cytometry. Additionally, mouse bone marrow cells derived macrophages (mBMMacs) and also human peripheral blood mononuclear cells (PBMCs) derived macrophages were stimulated with IL-4 and treated with muscarinic M3 receptor antagonist in vitro. The number of total cells and eosinophils, and the levels of cytokines (IL-5 and IL-13) in BALF were significantly decreased in asthma group treated with tiotropium compared to untreated asthma group. The expression of Relm-α and Arginase-1 in macrophages was significantly reduced in asthma group treated with tiotropium compared to untreated asthma group, suggesting that the development of M2 macrophages was inhibited by muscarinic M3 receptor blockage. The blockage of muscarinic M3 receptor in vitro, significantly inhibited the development of M2 macrophages in both mBMMacs and PBMCs derived macrophages. These results suggest that the blockage of muscarinic M3 receptor inhibits the development of M2 macrophages and prevent the allergic airway inflammation." @default.
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• W2912591195 date "2019-02-01" @default.
• W2912591195 modified "2023-09-26" @default.
• W2912591195 title "The effect of muscarinic M3 receptor blockage in development of M2 macrophages in allergic inflammation" @default.
• W2912591195 doi "https://doi.org/10.1016/j.jaci.2018.12.896" @default.
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