A New Mechanism of Pulmonary Fibrosis by Alveolar Macrophage Activation of Basophils

2021 Fiscal Year Final Research Report

• Project/Area Number: 18K15919
• Research Category: Grant-in-Aid for Early-Career Scientists
• Allocation Type: Multi-year Fund
• Review Section: Basic Section 53030:Respiratory medicine-related
• Research Institution: Tokyo Medical and Dental University
• Principal Investigator: Tateishi Tomoya 東京医科歯科大学, 東京医科歯科大学病院, 講師 (40645636)
• Project Period (FY): 2018-04-01 – 2022-03-31
• Keywords: ARDS / 好塩基球 / マクロファージ / 好中球

Outline of Final Research Achievements

Acute Rapid Respiratory Distress Syndrome (ARDS) is a poor prognosis disease characterized by a rapid inflammatory response to cytokine storms associated with pulmonary and systemic inflammation. However, the pathophysiology has not been clearly defined. In this study, we investigated the relationship between basophils and the pathogenesis of ARDS.
IL4 has been known to be a cytokine associated with ARDS. In our study, we found that removal of basophils aggravated or delayed the pathogenesis of ARDS as well as in IL4-deficient mice.
Network analysis by FACS and single-cell analysis suggested that IL4 produced by basophils is involved in macrophages and neutrophils.

Free Research Field

呼吸器内科学

Academic Significance and Societal Importance of the Research Achievements

好塩基球は白血球中の1%に過ぎない微量の細胞であるが，IL-4などのサイトカインを調整する重要な細胞である．この細胞が今回肺における炎症に影響を及ぼしていることが推定された．今後の研究によりこの細胞の活性化や，この細胞の出しているサイトカインを補充することが肺の炎症改善につながることが期待される．