巨噬细胞
炎症
串扰
收缩性
细胞因子
促炎细胞因子
巨噬细胞移动抑制因子
基质金属蛋白酶
败血症
细胞生物学
免疫学
医学
生物
内科学
体外
生物化学
物理
光学
作者
Zhi Li,Amy E. Bryant,Tanyalak Parimon,Dennis L. Stevens
出处
期刊:Cytokine
[Elsevier]
日期:2012-07-01
卷期号:59 (1): 191-194
被引量:6
标识
DOI:10.1016/j.cyto.2012.03.023
摘要
Myocardial dysfunction in group A streptococcal (GAS) toxic shock syndrome (StrepTSS) is characterized by severe biventricular dilatation and a striking reduction in ventricular performance; however, the mechanisms have not been fully elucidated. We have previously shown that pro-inflammatory cytokines are upregulated in the hearts of experimental animals with GAS bacteremia and that cardiomyocytes themselves as well as macrophages are the principal cytokine sources. Although macrophage-derived cytokines can clearly affect cardiac contractility, we questioned whether soluble cardiomyocyte-derived mediators might in turn affect macrophage function. Thus, we sought evidence of cardiomyocyte-to-macrophage directional cross-talk under resting versus GAS-stimulated conditions, using production of matrix metalloproteinase-9 (MMP-9) as an indicator of such signaling. Our results demonstrate that unstimulated cardiomyocytes produce a soluble inhibitor/s that maintains macrophage functional quiescence. Further, viable GAS induced production of cardiomyocyte-derived stimulator/s that overcomes quiescence and boosts macrophages production of MMP-9 and expression of pro-inflammatory cytokines (IL-1β, IL-6) and cardiodepressant factors (iNOS). Understanding the role of these cardiomyocyte-derived effectors of macrophage function (herein termed "cardiokines") in sepsis-associated cardiomyopathy may suggest new targets for therapeutic intervention.
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