Tissue macrophages are responsible for inflammatory liver disease in the hepatitis C virus transgenic mice

2015 Fiscal Year Final Research Report

• Project/Area Number: 24390117
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Partial Multi-year Fund
• Section: 一般
• Research Field: Virology
• Research Institution: Tokyo Metropolitan Institute of Medical Science
• Principal Investigator: KOHARA Michinori 公益財団法人東京都医学総合研究所, ゲノム医科学研究分野, プロジェクトリーダー (10250218)
• Co-Investigator(Kenkyū-buntansha): HIRATA Yuichi 公益財団財団法人東京都医学総合研究所, ゲノム医科学研究分野, 研究員 (50439452) ; YASUI Fumihiko 公益財団財団法人東京都医学総合研究所, ゲノム医科学研究分野, 主席研究員 (40399473) ; MUNAKATA Tsubasa 公益財団財団法人東京都医学総合研究所, ゲノム医科学研究分野, 主席研究員 (50420237)
• Project Period (FY): 2012-04-01 – 2016-03-31
• Keywords: C型肝炎ウイルス / 持続感染化 / 宿主免疫応答 / ウイルス排除

Outline of Final Research Achievements

We have reported that hepatitis C virus transgenic mice (HCV Tg) caused continuous liver injury and developed hepatocellular carcinoma through the Cre/loxP switching system. In addition, we showed recombinant vaccinia viruses expressing HCV nonstructural protein (rVV-N25) could protect against the progression of chronic hepatitis by way of suppression of macrophages activation. We focused on the role of tissue macrophages for liver disease of the HCV Tg mice and examined characteristic features of macrophages following rVV-N25 treatment. rVV-N25 treatment suppressed cell number and cytokine production on macrophages in the liver. M2 macrophages contribute to the induction of chronic liver inflammation in HCV mouse models. In addition, rVV-N25 induced therapeutic effect on liver tissue due to suppressed macrophage recruitment and activation.

Free Research Field

感染免疫