The role of claudins in the lung fibrosis post influenza virus-induced acute lung injury

2015 Fiscal Year Final Research Report

• Project/Area Number: 25860825
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Infectious disease medicine
• Research Institution: Tohoku University
• Principal Investigator: Aoyagi Tetsuji 東北大学, 医学(系)研究科(研究院), 講師 (50581609)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: 急性肺傷害 / 繊維化 / Influenza virus / Lipopolysaccharides / Claudin / Microparticles

Outline of Final Research Achievements

The clinical course and pathophysiological feature of ARDS are characterized as three phases: acute exduative, proliferative and fibrotic. We investigated the role of claudins, a family of proteins in the components of the tight junction, in acute and fibrotic phase of lung injury. We induced nonviral ARDS by alpha-galactosylceramide(GalCer) and LPS and viral ARDS by influenza virus infection. Claudin-5 and -18 are expressed in naive lungs. In both ARDS model, expression of claudin-4 was elevated and claudin-18 mRNA decreased in acute phases of lung injury. Claudin-4 was expressed in not only epithelial cells but leukocytes recruited into the lungs. Micorparticles in BAL fluid after influenza virus infection was observed. Influenza virus induced MPs have a potential to induced the cytokines and chemokines in alveolar machrophasge. These results indicated that claudins may be involved in the pathogenesis of acute phase of lung injury.

Free Research Field

臨床感染症