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Role of adhesion molecules and inflammation in Venezuelan equine encephalitis virus infected mouse brain

机译:黏附分子和炎症在委内瑞拉马脑炎病毒感染小鼠脑中的作用

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Background Neuroinvasion of Venezuelan equine encephalitis virus (VEEV) and subsequent initiation of inflammation in the brain plays a crucial role in the outcome of VEEV infection in mice. Adhesion molecules expressed on microvascular endothelial cells in the brain have been implicated in the modulation of the blood brain barrier (BBB) and inflammation in brain but their role in VEEV pathogenesis is not very well understood. In this study, we evaluated the expression of extracellular matrix and adhesion molecules genes in the brain of VEEV infected mice. Findings Several cell to cell adhesion molecules and extracellular matrix protein genes such as ICAM-1, VCAM-1, CD44, Cadherins, integrins, MMPs and Timp1 were differentially regulated post-VEEV infection. ICAM-1 knock-out (IKO) mice infected with VEEV had markedly reduced inflammation in the brain and demonstrated a delay in the onset of clinical symptoms of disease. A differential regulation of inflammatory genes was observed in the IKO mice brain compared to their WT counterparts. Conclusions These results improve our present understanding of VEEV induced inflammation in mouse brain.
机译:背景委内瑞拉马脑炎病毒(VEEV)的神经入侵和随后脑部炎症的引发在小鼠VEEV感染的结果中起着至关重要的作用。在大脑中的微血管内皮细胞上表达的粘附分子已经牵涉到脑中血脑屏障(BBB)和炎症的调节,但是它们在VEEV发病机理中的作用还不是很清楚。在这项研究中,我们评估了VEEV感染小鼠的大脑中细胞外基质和粘附分子基因的表达。研究发现VEEV感染后,一些细胞间粘附分子和细胞外基质蛋白基因(如ICAM-1,VCAM-1,CD44,Cadherins,整联蛋白,MMP和Timp1)受到差异调节。感染VEEV的ICAM-1敲除(IKO)小鼠显着减少了脑部炎症,并显示了疾病临床症状发作的延迟。与野生型WT小鼠相比,在IKO小鼠的大脑中观察到了炎症基因的差异调节。结论这些结果改善了我们目前对VEEV引起的小鼠大脑炎症的了解。

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