【摘 要】
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Background The inflammatory response plays a critical role in hypertensioninduced cardiac remodeling.We aimed to study how interaction among inflammatory cells causes inflammatory responses in the pro
【机 构】
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Beijing An Zhen Hospital, Capital Medical University
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Background The inflammatory response plays a critical role in hypertensioninduced 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 γ (IFN γ) and leukocytes infiltration into the heart.To determine the role of IFN γ c on cardiac inflammation and remodeling,both wild—type (WT) and IFNeknockout (KO) mice were infused Ang Ⅱ for 7 days,and were found an equal blood pressure increase.However,knockout of IFNγ prevented Ang Ⅱinduced:1) infiltration of macrophages and T cells into cardiac tissue; 2) expression of tumor necrosis factor a and monocyte chemoattractant protein 1 (MCP1),and 3) cardiac fibrosis,including the expression of asmooth muscle actin and collagen Ⅰ (all p,0.05).Cultured T cells or macrophages alone expressed very low level of IFN γ,however,coculture of T cells and macrophages increased IFN γ expression.In vitro coculture studies using T cells and macrophages from WT or IF N γ KO mice demonstrated that T cells were primary source for lFNγ production.Coculture of WT macrophages with WT T cells,but not with IFN γknockout T cells,increused IFN γ production.Moreover,IFN γ produced by T cells amplified MCP1 expression in macrophages and stimulated macrophage migration.
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