关键词: ACh, acetylcholine IP, intraperitoneal ISP, intracellular sigma peptide MI, myocardial infarction NE, norepinephrine PBS, phosphate-buffered saline TH, tyrosine hydroxylase Tregs, regulatory T cells VEH, vehicle inflammation mIHC, multiplex immunohistochemistry macrophages multiplex IHC myocardial infarction sympathetic nervous system β1-AR, adrenergic receptor

来  源:   DOI:10.1016/j.jacbts.2022.04.009   PDF(Pubmed)

Abstract:
Myocardial infarction (MI) triggers an inflammatory response that transitions from pro-inflammatory to reparative over time. Restoring sympathetic nerves in the heart after MI prevents arrhythmias. This study investigated if reinnervation altered the immune response after MI. This study used quantitative multiplex immunohistochemistry to identify the immune cells present in the heart 2 weeks after ischemia-reperfusion. Two therapeutics stimulated reinnervation, preventing arrhythmias and shifting the immune response from inflammatory to reparative, with fewer pro-inflammatory macrophages and more regulatory T cells and reparative macrophages. Treatments did not alter macrophage phenotype in vitro, which suggested reinnervation contributed to the altered immune response.
摘要:
心肌梗塞(MI)引发炎症反应,随着时间的推移从促炎转变为修复性。MI后恢复心脏交感神经可预防心律失常。这项研究调查了神经支配是否改变了MI后的免疫反应。本研究使用定量多重免疫组织化学来鉴定缺血再灌注2周后心脏中存在的免疫细胞。两种疗法刺激神经支配,预防心律失常并将免疫反应从炎症转变为修复,更少的促炎巨噬细胞和更多的调节性T细胞和修复性巨噬细胞。治疗在体外没有改变巨噬细胞表型,这表明神经支配有助于改变免疫反应。
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