Mechanism elucidation of M2 macrophages activation via complements and therapeutic application for difficult to treat and neutrophilic asthma

2021 Fiscal Year Final Research Report

• Project/Area Number: 20K17235
• Research Category: Grant-in-Aid for Early-Career Scientists
• Allocation Type: Multi-year Fund
• Review Section: Basic Section 53030:Respiratory medicine-related
• Research Institution: Kurume University
• Principal Investigator: Tokunaga Yoshihisa 久留米大学, 医学部, 助教 (60832722)
• Project Period (FY): 2020-04-01 – 2022-03-31
• Keywords: 気管支喘息 / マクロファージ / サブセット

Outline of Final Research Achievements

The CD163 positive M2-like macrophages counts in the lung tissue in patients with fatal asthma group were significantly increased when compared with those in non-asthma patients control group. In the mouse model, airway hyperresponsibility significantly suppressed and and decreased the number of neutrophils and eosinophils in bronchoalveolar lavage fluid (BALF) in M2-like macrophage knock-out mice when compared with those with the wild type mice. In BALF % of macrophages were associated with % of neutrophils (r = -0.97, P <0.0001). Our results suggest that the enhancements of M2-like macrophage may be associated with developments of difficult-to treat neutrophilic asthma. However, we could not clarify the relationship between complements and M2-like macrophage, and neutrophilic inflammations.

Free Research Field

呼吸器内科

Academic Significance and Societal Importance of the Research Achievements

日本では重症ぜん息と考えられているのは約50万から100万人いると推測されている。好中球性ぜん息は、非タイプ２ぜん息として、治療に難渋することが多いとされる。わたしたちの結果は、好中球性ぜん息の病態解明に貢献し、新たな治療法の開発に役立つと考えられる。