reciprocal interaction between macrophages and t cells stimulates ifn-γ and mcp-1 production in ang ii-induced cardiac inflammation and fibrosis相互之间的交互巨噬细胞和t细胞刺激ifn-γmcp-1生产和ii-induced心脏炎症和纤维化.pdfVIP

Reciprocal Interaction between Macrophages and T cells Stimulates IFN-c and MCP-1 Production in Ang II-induced Cardiac Inflammation and Fibrosis 1 1 1 1 1,2 1,2 1,2 Ya-lei Han , Yu-lin Li , Li-xin Jia , Ji-zhong Cheng , Yong-fen Qi , Hong-jia Zhang , Jie Du * 1 Beijing An Zhen Hospital, Capital Medical University, Beijing, China, 2 The Key Laboratory of Remodeling-related Cardiovascular Diseases, Ministry of Education, Institute of Heart Lung and Blood Vessel Diseases, Beijing, China Abstract Background: The inflammatory response plays a critical role in hypertension-induced cardiac remodeling. We aimed to study how interaction among inflammatory cells causes inflammatory responses in the process of hypertensive cardiac fibrosis. Methodology/Principal Findings: Infusion of angiotensin II (Ang II, 1500 ng/kg/min) in mice rapidly induced the expression of interferon c (IFN-c) and leukocytes infiltration into the heart. To determine the role of IFN-c on cardiac inflammation and remodeling, both wild-type (WT) and IFN-c-knockout (KO) mice were infused Ang II for 7 days, and were found an equal blood pressure increase. However, knockout of IFN-c prevented Ang II-induced: 1) infiltration of macrophages and T cells into cardiac tissue; 2) expression of tumor necrosis factor a and monocyte chemoattractant protein 1 (MCP-1), and 3) cardiac fibrosis, including the expression of a-smooth muscle actin and collagen I (all p,0.05). Cultured T cells or macrophages alone expressed very low level of IFN-c, however, co-culture of T cells and macrophages increased IFN-c expression by 19.860.95 folds (vs.