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首页> 美国卫生研究院文献>Aging and Disease >Inflammatory Cytokines Induce Expression of Chemokines by Human Retinal Cells: Role in Chemokine Receptor Mediated Age-related Macular Degeneration
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Inflammatory Cytokines Induce Expression of Chemokines by Human Retinal Cells: Role in Chemokine Receptor Mediated Age-related Macular Degeneration

机译：炎性细胞因子诱导人视网膜细胞趋化因子的表达：在趋化因子受体介导的年龄相关性黄斑变性中的作用。

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Chemokine reeptor-3 (CCR-3) was shown to be associated with choroidal neovascularization (CNV) in age-related macular degeneration (AMD). AMD is a vision threatening retinal disease that affects the aging population world-wide. Retinal pigment epithelium and choroid in the posterior part of the retina are the key tissues targeted in the pathogenesis of CNV in AMD. We used human retinal pigment epithelial (HRPE) and choroidal fibroblast (HCHF) cells, prepared from aged adult human donor eyes, to evaluate the expression of major CCR-3 ligands, CCL-5, CCL -7, CCL-11,CCL-24 and CCL-26. Microarray analysis of gene expression in HRPE cells treated with inflammatory cytokine mix (ICM= IFN-γ+TNF-α+IL-1β) revealed 75 and 23-fold increase in CCL-5 and CCL-7 respectively, but not CCL-11, CCL-24 and CCL-26. Chemokine secretion studies of the production of CCL5 and CCL7 by HRPE corroborated with the gene expression analysis data. When the HRPE cells were treated with either individual cytokines or the ICM, both CCL-5 and CCL-7 were produced in a dose dependent manner. Similar to the gene expression data, the ICM did not enhance HRPE production of CCL-11, CCL-24 and CCL-26. CCL-11 and CCL-26 were increased with IL-4 treatment and this HRPE production was augmented in the presence of TNF-α and IL1β. When HCHF cells were treated with either individual cytokines or the ICM, both CCL-5 and CCL-7 were produced in a dose dependent fashion. IL-4 induced low levels of CCL-11 and CCL-26 in HCHF and this production was significantly enhanced by TNF-α. Under these conditions, neither HRPE nor HCHF were demonstrated to produce CCL-24. These data demonstrate that chronic inflammation triggers CCL-5 and CCL-7 release by HRPE and HCHF and the subsequent interactions with CCR3 may participate in pathologic processes in AMD.
机译：在年龄相关性黄斑变性（AMD）中，趋化因子受体3（CCR-3）与脉络膜新生血管（CNV）相关。 AMD是一种威胁视力的视网膜疾病，会影响世界范围内的老龄化人口。视网膜后部的视网膜色素上皮和脉络膜是AMD中CNV发病机制的关键组织。我们使用从成年成人供体眼睛制备的人视网膜色素上皮细胞（HRPE）和脉络膜成纤维细胞（HCHF）细胞来评估主要CCR-3配体，CCL-5，CCL -7，CCL-11，CCL- 24和CCL-26。基因芯片在炎症细胞因子混合物（ICM =IFN-γ+TNF-α+IL-1β）处理的HRPE细胞中的基因表达的微阵列分析显示，CCL-5和CCL-7分别增加了75倍和23倍，而CCL-11没有，CCL-24和CCL-26。 HRPE产生CCL5和CCL7的趋化因子分泌研究与基因表达分析数据相符。当用单个细胞因子或ICM处理HRPE细胞时，CCL-5和CCL-7均以剂量依赖性方式产生。与基因表达数据相似，ICM不能增强CCL-11，CCL-24和CCL-26的HRPE产生。 IL-4处理可增加CCL-11和CCL-26，而在TNF-α和IL1β的存在下，HRPE的产生会增加。当用单个细胞因子或ICM处理HCHF细胞时，CCL-5和CCL-7均以剂量依赖性方式产生。 IL-4诱导HCHF中低水平的CCL-11和CCL-26，TNF-α显着增强了这种产生。在这些条件下，HRPE和HCHF均未产生CCL-24。这些数据表明，慢性炎症触发了HRPE和HCHF释放CCL-5和CCL-7，并且随后与CCR3的相互作用可能参与了AMD的病理过程。

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