Interactions between HIV‐infected monocytes and the extracellular matrix: increased capacity of HIV‐infected monocytes to adhere to and spread on extracellular matrix associated with changes in extent of virus replication and cytopathic effects in infected cells

Interactions between HIV‐infected monocytes and the extracellular matrix: increased capacity of HIV‐infected monocytes to adhere to and spread on extracellular matrix associated with changes in extent of virus replication and cytopathic effects in infected cells
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HIV感染的单核细胞与细胞外基质之间的相互作用:HIV感染的单核细胞在细胞外基质上粘附和扩散的能力增加,与感染细胞中病毒复制程度和细胞病变效应的变化相关

DOI:
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发表时间:
1992
影响因子:
5.5
通讯作者:
M. Meltzer
M. Meltzer
中科院分区:
医学3区
文献类型:
--
作者:
S. Dhawan;Maurann Vargo;M. Meltzer

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单核细胞表达基底膜细胞外基质 (ECM) 蛋白的细胞表面受体。这些受体在细胞通过毛细血管内皮外渗到组织的过程中起作用。粘附在 ECM 上超过 2 小时的人类免疫缺陷病毒 (HIV) 感染的单核细胞数量是未感染的对照细胞的三倍。这种差异是 ECM 特异性的,在牛血清白蛋白底物中未观察到这种差异。 HIV 感染后 4 天,单核细胞对 ECM 的粘附力明显增强,并在 10 天后增强。暴露于 T 细胞嗜性 HIV 毒株的单核细胞与单核细胞结合但不在其中复制,显示对 ECM 的粘附没有变化。因此,HIV对单核细胞的有效感染会导致这些细胞与ECM相互作用的能力显着增加。 HIV 感染的单核细胞对 ECM 的粘附增强与扩散的增加​​有关:12 小时时,在 ECM 上扩散的 HIV 感染的单核细胞比未感染的对照细胞多六倍。感染 HIV 的单核细胞的细胞过程在 ECM 上形成了一个复杂的网络:通过间接免疫荧光检测,许多细胞表达 HIV 蛋白。 HIV 相关的细胞病变效应和病毒粒子相关逆转录酶活性的水平取决于单核细胞附着的底物。粘附于 ECM、纤连蛋白或单独塑料的单核细胞中的病毒复制和细胞病变效应是相当的。相比之下,感染 HIV 的单核细胞在感染后 2 周内病毒复制和细胞病变效应显着增加。 HIV 复制和细胞病变效应水平最低的是附着于 IV 型胶原的单核细胞。单核细胞和 ECM 之间的相互作用深刻影响这些细胞控制 HIV 感染的方式:HIV 感染改变了受感染单核细胞在 ECM 上附着和传播的能力;与 ECM 的附着改变了受感染细胞中病毒复制的程度。
Monocytes express cell surface receptors for extracellular matrix (ECM) proteins of basement membranes. These receptors are engaged during extravasation of cells through capillary endothelium into tissue. The number of human immunodeficiency virus (HIV)‐infected monocytes that adhered to ECM over 2 h was threefold higher than that of uninfected control cells. This difference was ECM specific and was not observed with a bovine serum albumin substrate. Enhanced adhesion to ECM was evident in monocytes by 4 days after HIV infection and increased through 10 days. Monocytes exposed to a T cell–tropic HIV strain that binds to but does not replicate in monocytes showed no changes in adherence to ECM. Thus, productive infection of monocytes by HIV induces a significant increase in the capacity of these cells to interact with ECM. Enhanced adhesion of HIV‐infected monocytes to ECM was associated with increased spreading: at 12 h, sixfold more HIV‐infected monocytes were spread on ECM than were uninfected control cells. Cell processes of HIV‐infected monocytes formed a complex network on ECM: many of these cells expressed HIV proteins as detected by indirect immunofluorescence. HIV‐associated cytopathic effects and levels of virion‐associated reverse transcriptase activity depended on the substrate to which monocytes were attached. Virus replication and cytopathic effects in monocytes adhered to ECM, fibronectin, or plastic alone were comparable. In contrast, HIV‐infected monocytes attached to laminin showed a significant increase in virus replication and in extent of cytopathic effects through 2 weeks after infection. The lowest levels of HIV replication and cytopathic effects were in monocytes attached to collagen IV. Interactions between monocytes and ECM profoundly affect the manner in which these cells control HIV infection: HIV infection changes the capacity of infected monocytes to attach and spread on ECM; attachment to ECM alters the extent of virus replication in infected cells.
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DOI: --
发表时间: 1987
期刊: Journal of immunology (Baltimore, Md. : 1950)
影响因子: --
作者:
Fuhlbrigge,RC;Chaplin,DD;Kiely,JM;Unanue,ER
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DOI: --
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期刊: Journal of immunology (Baltimore, Md. : 1950)
影响因子: --
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DOI: 10.1073/pnas.88.15.6632
发表时间: 1991
影响因子: 11.1
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Skolnik,PR;Jahn,B;Wang,MZ;Rota,TR;Hirsch,MS;Krane,SM
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DOI: --
发表时间: 1988
期刊: Journal of immunology (Baltimore, Md. : 1950)
影响因子: --
作者:
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