The therapeutic strategy for burn-induced immunosuppression: Regulation of phagocytes function.

2016 Fiscal Year Final Research Report

• Project/Area Number: 26462773
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Emergency medicine
• Research Institution: National Defense Medical College
• Principal Investigator: MIYAZAKI Hiromi 防衛医科大学校(医学教育部医学科進学課程及び専門課程、動物実験施設、共同利用研究, 防衛医学研究センター, 助教 (30531636)
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: 侵襲 / 活性酸素 / 好中球 / 貪食活性

Outline of Final Research Achievements

Although reactive oxygen species (ROS) basically play beneficial roles to maintain host homeostasis against external disturbance including infection, excessive ROS generation by activated neutrophils can cause organ damage. We investigated the role of burn-induced ROS generation in the injured hosts, focusing on postburn infection. Inhibition of the ROS production during/immediately after injury did not improve the burn-induced susceptibility to infection or the neutrophil dysfunction. Interestingly, inhibition of the subsequent ROS production potently restored the neutrophil functions and hematopoietic function of the bone marrow cells, thereby improving the postburn infection. Although the inhibition of burn-evoked ROS generation is effective against burn-induced organ injury, it may be ineffective against postburn infection. Preservation of the immediate burn-evoked ROS production, but the inhibition of subsequent ROS production, may be crucial to protect against postburn infection.

Free Research Field

救急医学