The role of autophagy in severe influenza-related pneumonia

Research Project

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
Project Status	Completed (Fiscal Year 2017)
Budget Amount *help	¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000) Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000) Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000) Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Keywords	インフルエンザウイルス / 肺炎球菌 / オートファジー / オートファジー阻害薬
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.