期刊
AMERICAN JOURNAL OF PATHOLOGY
卷 165, 期 6, 页码 1883-1894出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/S0002-9440(10)63241-5
关键词
-
类别
资金
- NHLBI NIH HHS [HL70729, R01 HL070729, R01 HL067290, HL67290] Funding Source: Medline
- NIAID NIH HHS [R21 AI051835, AI51835] Funding Source: Medline
Inflammatory fibrosis is a characteristic feature of myocarditis, dilated cardiomyopathy (I)CM), and congestive heart failure. Th1-type immune responses, mediated by interleukin (IL)-12-induced interferon (IFN)-gamma, are believed to exacerbate autoimmune diseases including myocarditis. in this study, we examined the effect of IL-12Rbeta1 and IFN-gamma deficiency on the development of chronic CB3-induced myocarditis using knockout mice. We found increased chronic CB3-induced myocarditis (14.1 to 43.1%, P < 0.001); pericarditis (1.5 to 7.6%, P < 0.001); fibrosis (9.7 to 27.4%, P < 0.05); and the profibrotic cytokines transforming growth factor-beta(1), IL-1beta, and IL-4 in the hearts of IFN-gamma-deficient mice. All mice infected with CB3 developed DCM, but IFN-gamma-deficient mice developed a fibrous, adhesive pericarditis associated with increased numbers of degranulating mast cells (MCs) in the pericardium (26.6 to 45.9%, P < 0.01), increased histamine levels (716 to 1930 ng/g of heart, P < 0.01), and reduced survival (100 to 43%). In contrast, IL-12Rbeta1 deficiency did not significantly alter the development of chronic myocarditis. Thus, IFN-gamma protects against the development of severe chronic myocarditis, pericarditis, and DCM after CB3 infection by reducing MC degranulation, fibrosis, and the profibrotic cytokines transforming growth factor-beta(1), IL-1beta, and IL-4 in the heart.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据