Characterization of cytokine and iNOS mRNA expression in situ during the course of experimental autoimmune myocarditis in rats
Characterization of cytokine and iNOS mRNA expression in situ during the course of experimental autoimmune myocarditis in rats
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DOI：
10.1006/jmcc.1996.0293
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发表时间：
1997-02-01
影响因子：
5
通讯作者：
Abo, T
中科院分区：
文献类型：
--
作者：
Okura, Y;Yamamoto, T;Abo, T
采用核糖核酸酶过程保护法检测实验性自身免疫性心肌炎（EAM）大鼠心肌中几种细胞因子、诱导型NO合成酶（iNOS）、构成型内皮NO合成酶（cNOS）和穿孔素的mRNA表达。白细胞介素2 （IL-2）在炎症初期（第14天）出现，在炎症最严重期（第19天）消退，在恢复期（第25天）消失。IL-1 β、干扰素γ和肿瘤坏死因子α (tnf - α) mRNA仅在最大炎症期检测到，iNOS也在此期间出现了数天。相比之下，IL-10 mRNA在最大炎症期后检测到，并持续到恢复期（25-36天）。虽然转化生长因子β 1 （tgf - β 1）在所有阶段均可检测到，但在炎症最严重阶段表达明显增强，并逐渐降低（约36天）至基础水平，但在疾病的任何阶段均未检测到穿孔素mRNA。除了巨噬细胞和CD4(+) T细胞外，心肌中还发现了大量中性粒细胞，尤其是在炎症高峰期。我们认为抗原（Ag）引发的Ag呈递细胞或巨噬细胞与T细胞（Th-1）相互作用产生IL-2和随后的ifn - γ，从而进一步激活心肌中的巨噬细胞。因此，tnf - α和iNOS可能对心肌造成组织损伤，也表明tgf - β 1和一种代表性的Th-2细胞因子IL-10有助于抑制炎症。这些结果表明，在EAM的不同阶段产生Th-1和Th-2细胞因子，并调节炎症和EAM的过程。(C) 1997学术出版社有限公司
Course of Ribonuclease protection assay was used to demonstrate mRNA expression of several cytokines as well as inducible NO synthase (iNOS), constitutive endothelial NO synthase (cNOS) and perforin in the myocardium during the course of experimental autoimmune myocarditis (EAM) in rats. Interleukin 2 (IL-2) appeared in the initial inflammatory phase (day 14), subsided in the maximum inflammatory phase (day 19) and disappeared by the recovery phase (day 25). mRNA of IL-1 beta, interferon gamma INF-gamma and tumor necrosis factor alpha (TNF-alpha) were detected only in the maximum inflammatory phase and iNOS also appeared for several days at this time. In contrast, IL-10 mRNA was detected after the maximum inflammatory stage and persisted into the recovery phase (days 25-36). Although transforming growth factor beta 1 (TGF-beta 1) could be detected in all phases, the expression was markedly enhanced in the maximum inflammatory phase and gradually diminished (around day 36) to basal levels, Perforin mRNA was not detected at any point in the disease. Besides macrophages and CD4(+) T cells, a number of neutrophils were found in the myocardium, especially at peak inflammatory stage. We suggest that antigen (Ag) primed Ag presenting cells or macrophages interact with T cells (Th-1) to produce IL-2 and subsequent IFN-gamma, which further activates macrophages in the myocardium. Consequently, TNF-alpha and iNOS may inflict tissue damage to myocardium, It is also suggested that TGF-beta 1 and one representative Th-2 cytokine, IL-10, help inhibit inflammation. These findings suggest that Th-1 and Th-2 cytokines are produced at different stages of EAM and modulate the inflammation and the course of EAM. (C) 1997 Academic Press Limited.