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Viral infection and Cardiomyopathy: enteroviral Replication and Cardiocyte Injury in the Recipient Hearts of Dilated Cardiomyopathy and Perforin Knockout Mice with Viral Myocarditis

病毒感染与心肌病：扩张型心肌病和穿孔素敲除小鼠病毒性心肌炎受体心脏中的肠道病毒复制和心肌细胞损伤

基本信息

批准号：
13670757
负责人：
DEGUCHI Hirofumi
金额：
$ 0.19万
依托单位：
Osaka Medical College
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2001
资助国家：
日本
起止时间：
2001 至 2002
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-13670757/
关键词：
Dilated cardiomyopathy Cardiac transplantation Viral myocarditis Coxsackievirus Cytokine Perforin Knockout mouse PCR

项目摘要

(A) Enteroviral detection and cytokine expression in the recipient hearts from patients with dilated cardiomyopathy (DCM)We examined myocardial specimens obtained from 30 DCM patients who underwent heart transplantation.(1) Semiquantitative analysis of histological findings: histological findings showed inflammatory cell infiltration in 14DCM patients (47%) and fibrosis in 18 patients (60%). 4 patients (13%) had active myocarditis.(2) Cytokine expression in the heart: We elucidated the expression of inflammatory cytokine in the recipient hearts using the ABI PRISM7700. IL-1β mRNA was overexpressed in 5 of 12 DCM patients (42%), and IL-8 in 5 of 12 (42%). Expression of IL-12p35, IL15 and IFN-γ mRNA raised respectively in 1 of 12 patients (8%). The findings suggest IL-1β and IL-8 play significant role in the inflammatory lesion in the myocardium of DCM.(B) Experimental Coxsackievirus B3 Myocarditis in Perforin Knockout (pfk) MiceWe examined light and electron microscopic (EM) changes of the myocardium obtained from pfk and wild (C57BL/6) mice with Coxsackievirus B3 myocarditis. In wild mice many cardiocytes underwent necrosis with infiltration of lymphocytes and macrophages. By immuno EM perforin were often observed in the granules of lymphocytes. These lymphocytes showed close contact with cardiocytes. In pfk mice cardiocyte necrosis was less than in wild mice, although significant number of lymphocytes infiltrated in the myocardium. These findings suggest that pfk plays an important role in the development of lymphocyte-mediated cardiocyte injury.

(A)扩张型心肌病(DCM)患者受体心脏肠道病毒检测及细胞因子表达我们检测了30例DCM患者心脏移植后的心肌标本。(1)组织学半定量分析：14例DCM患者(47%)组织学表现为炎性细胞浸润(47%)，18例(60%)为纤维化。活动性心肌炎4例(13%)。(2)细胞因子在心脏中的表达：我们用ABI PRISM7700分析了炎性细胞因子在受体心脏中的表达。IL-1和IL-8在12例扩张型心肌病患者中分别有5例(42%)和5例(42%)呈β高表达。IL-12p35、IL-15和干扰素-γ基因表达分别升高1例(8%)。本研究结果提示IL-1、β和IL-8在扩张型心肌炎心肌炎性病变中起重要作用。(2)柯萨奇病毒B3型心肌炎穿孔素基因敲除小鼠的实验性心肌炎。在野生小鼠，许多心肌细胞坏死，淋巴细胞和巨噬细胞浸润。免疫组织化学显示，淋巴细胞颗粒内可见穿孔素。这些淋巴细胞与心肌细胞密切接触。尽管有大量淋巴细胞渗入心肌，但PFK组小鼠的心肌细胞坏死率低于野生组。这些发现表明，PFK在淋巴细胞介导的心肌细胞损伤的发生发展中起重要作用。