Phenotypic variation in myocardial macrophage populations suggests a role for macrophage activation in SIV-associated cardiac disease.
Phenotypic variation in myocardial macrophage populations suggests a role for macrophage activation in SIV-associated cardiac disease.
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心肌巨噬细胞群体的表型变异表明巨噬细胞活化在 SIV 相关心脏病中发挥作用。
DOI：
10.1089/aid.2006.0211
复制
发表时间：
2007
影响因子：
1.5
通讯作者：
Mansfield,KeithG
中科院分区：
文献类型：
--
作者：
Yearley,JenniferH;Pearson,Christine;Shannon,RichardP;Mansfield,KeithG
心脏异常在艾滋病毒感染者中很常见，并且作为艾滋病毒感染儿童死亡的原因，已经有充分的记录。hiv感染引起心肌疾病的潜在发病机制尚不完全清楚。siv感染的恒河猴出现了一系列类似于hiv感染者的心脏病变，为发病机制研究提供了一个重要的模型。对siv感染的恒河猴尸体解剖收集的心脏组织进行回顾性分析，以评估心肌巨噬细胞和树突状细胞群作为先前定量的淋巴细胞炎症浸润和心肌细胞变性或坏死的功能。巨噬细胞和树突状细胞群的大小和表型变化被检查为siv相关炎症病变发病机制的可能贡献者。免疫组织化学标记CD163的巨噬细胞与标记HAM56的巨噬细胞在总体数量、组间分布、参与炎症簇、与巨噬细胞DC-SIGN+亚群的相关性以及与siv感染细胞数量的相关性方面存在本质差异。CD163+巨噬细胞在siv感染动物未感染的心脏中的数量明显高于siv感染心肌炎动物或未感染对照组（p< 0.01）。CD163+细胞数量与siv感染细胞数量呈正相关（p< 0.05），提示CD163+群体与心脏内炎症浸润减少和病毒控制降低相关。由于CD163与非经典巨噬细胞活化和抗炎表型相关，这些结果表明，经典活化和非经典活化之间的平衡可能影响炎症浸润水平和心肌病毒负荷。
Cardiac abnormalities are common in HIV-infected individuals, and have been especially well documented as contributors to mortality in HIV-infected children. Underlying pathogenetic mechanisms responsible for myocardial disease in HIV-infection remain imperfectly understood. SIV-infected rhesus monkeys develop a spectrum of cardiac lesions similar to those seen in HIV-infected people, providing an important model for pathogenesis studies. Retrospective analysis of cardiac tissue collected at necropsy from SIV-infected rhesus monkeys was performed to evaluate myocardial macrophage and dendritic cell populations as a function of previously quantitated lymphocytic inflammatory infiltrates and cardiomyocyte degeneration or necrosis. Variations in the size and phenotype of macrophage and dendritic cell populations were examined as possible contributors to the pathogenesis of SIV-associated inflammatory lesions. Macrophages labeling immunohistochemically for CD163 differed substantially from macrophages labeling for HAM56 in overall number, distribution across groups, involvement in inflammatory clusters, correlation with the DC-SIGN+subpopulation of macrophages, and correlation with numbers of SIV-infected cells. CD163+macrophages occurred in significantly higher numbers in uninflamed hearts from SIV-infected animals than in hearts from SIV-infected animals with myocarditis or uninfected controls (p< 0.01). Numbers of CD163+cells correlated positively with numbers of SIV-infected cells (p< 0.05) suggesting that the CD163+population was associated with decreased inflammatory infiltration and reduced control of virus within the heart. As CD163 has been associated with nonclassical macrophage activation and an antiinflammatory phenotype, these results suggest that a balance between classical and nonclassical activation may affect levels of inflammatory infiltration and of myocardial virus burden.
DOI：
10.3758/bf03326763
发表时间：
1983
期刊：
Psychobiology
影响因子：
--
作者：
Sue B. Miller;M. Potegal;L. Abraham
通讯作者：
L. Abraham
高等脊椎动物行为的神经机制
影响因子：
1.3
作者：
Robert L. Isaacson;J. S. Beritoff (Beritashvili);W. T. Liberson
通讯作者：
W. T. Liberson