The study of pathophysiology and a role of group 2 innate lymphoid cells in virus-induced bronchial asthma

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K09665
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Pediatrics
• Research Institution: Tokai University
• Principal Investigator: KATO Masahiko 東海大学, 医学部, 准教授 (30292593)
• Co-Investigator(Kenkyū-buntansha): 林 泰秀 群馬県衛生環境研究所, 研究企画係, 研究員 (30238133) ; 山田 佳之 群馬県衛生環境研究所, 研究企画係, 研究員 (80309252) ; 望月 博之 東海大学, 医学部, 教授 (50270856)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: ウイルス感染 / 気管支喘息 / 好酸球 / サイトカイン

Outline of Final Research Achievements

To investigate the pathogenesis of acute exacerbations of asthma induced by viral infection, we examined bronchial resistance, peripheral blood and bronchial alveolar fluid (BALF) cells analyses and 23 types of cytokines/chemokines using an experimental asthma model mice infected with respiratory syncytial virus (RSV). The levels of BALF and tissue eosinophils showed significant increase in ovalbumin (OVA) and OVA/RSV groups compared with controls. MIP-1α in BALF was significantly increased in OVA/RSV groups compared with RSV groups, OVA groups, and control groups. Serum IL-5 in OVA groups and serum IL-17 in OVA/RSV groups were also higher than in controls. These findings suggest that eosinophilic inflammation via MIP-1α, IL-5, and IL-17 may play an important role in acute exacerbations of asthma model induced by RSV.

Free Research Field

小児アレルギー学