弓形虫可增强人视网膜色素上皮细胞中转化生长因子-β的表达：在视网膜脉络膜炎免疫发病机制中的潜在作用
Transforming growth factor-beta expression in human retinal pigment epithelial cells is enhanced by Toxoplasma gondii: a possible role in the immunopathogenesis of retinochoroiditis.
作者信息
Nagineni C N, Detrick B, Hooks J J
机构信息
Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892, USA.
出版信息
Clin Exp Immunol. 2002 May;128(2):372-8. doi: 10.1046/j.1365-2249.2002.01815.x.
Abstract
Retinochoroiditis caused by Toxoplasma gondii infection results in inflammation and necrosis of the retina. We have used human retinal pigment epithelial cultures (HRPE) as an in vitro model to investigate the role of TGF-beta in T. gondii-induced retinochoroiditis. RT-PCR analyses showed enhanced steady state levels of TGF-beta1 and TGF-beta2 mRNA in T. gondii-infected HRPE. Uninfected HRPE secrete TGF-beta1 in a latent form while 10-30% of the secreted TGF-beta2 was in the active form. T. gondii infection induced a significant increase (P < 0.01) in total TGF-beta1 and TGF-beta2 secretion by HRPE. In addition, soluble extracts of T. gondii (ST) stimulated secretion of both TGF-beta1 and TGF-beta2 significantly (P < 0.01). Interestingly, T. gondii infection as well as ST of the parasites completely inhibited secretion of the active form of TGF-beta2. Studies evaluating the effect of TGF-beta on T. gondii replication in HRPE revealed that TGF-beta enhanced parasite replication. The interactions between host retinal cells and T. gondii may play an active role in the pathogenesis of retinochoroiditis.
摘要
由弓形虫感染引起的视网膜脉络膜炎会导致视网膜发生炎症和坏死。我们使用人视网膜色素上皮细胞培养物（HRPE）作为体外模型，来研究转化生长因子-β（TGF-β）在弓形虫诱导的视网膜脉络膜炎中的作用。逆转录聚合酶链反应（RT-PCR）分析显示，在感染弓形虫的HRPE中，TGF-β1和TGF-β2信使核糖核酸（mRNA）的稳态水平增强。未感染的HRPE以潜伏形式分泌TGF-β1，而所分泌的TGF-β2中有10%-30%是活性形式。弓形虫感染导致HRPE分泌的总TGF-β1和TGF-β2显著增加（P<0.01）。此外，弓形虫的可溶性提取物（ST）显著刺激了TGF-β1和TGF-β2的分泌（P<0.01）。有趣的是，弓形虫感染以及寄生虫的ST完全抑制了活性形式的TGF-β2的分泌。评估TGF-β对HRPE中弓形虫复制影响的研究表明，TGF-β增强了寄生虫的复制。宿主视网膜细胞与弓形虫之间的相互作用可能在视网膜脉络膜炎的发病机制中发挥积极作用。
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