The role of autophagy in severe influenza-related pneumonia

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K19587
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Infectious disease medicine
• Research Institution: Nagasaki University
• Principal Investigator: KOSAI Kosuke 長崎大学, 病院(医学系), 助教 (70644433)
• Research Collaborator: YANAGIHARA Katsunori 長崎大学, 医歯薬学総合研究科(医学系), 教授 (40315239) ; MORINAGA Yoshitomo 長崎大学, 医歯薬学総合研究科(医学系), 助教 (30580360)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: インフルエンザウイルス / 肺炎球菌 / オートファジー

Outline of Final Research Achievements

We analyzed the role of autophagy in severe influenza-related bacterial pneumonia. In vitro studies showed that the number of A549 cells expressing autophagic vesicle increased during coinfection in a time-dependent manner, and decreased after they peaked. The expression of LC3B in inflammatory cells increased in coinfected mice, compared to uninfected mice. Autophagy inhibitor suppressed the gene and protein expression of interleukin (IL)-6 in coinfection in vitro, whereas it enhanced the expression of matrix metalloproteinase (MMP)-10. Autophagy may be involved in mechanisms of severe influenza-related bacterial pneumonia.

Free Research Field

感染症学、呼吸器病学