Aga Khan University, Stadium Road, Karachi, Pakistan.
Trends Parasitol. 2011 May;27(5):185-9. doi: 10.1016/j.pt.2011.01.005. Epub 2011 Apr 18.
Acanthamoeba granulomatous encephalitis generally develops as a result of haematogenous spread, but it is unclear how circulating amoebae enter the central nervous system (CNS) and cause inflammation. At present, the mechanisms which Acanthamoeba use to invade this incredibly well-protected area of the CNS and produce infection are not well understood. In this paper, we propose two key virulence factors: mannose-binding protein and extracellular serine proteases as key players in Acanthamoeba traversal of the blood-brain barrier leading to neuronal injury. Both molecules should provide excellent opportunities as potential targets in the rational development of therapeutic interventions against Acanthamoeba encephalitis.
棘阿米巴肉芽肿性脑炎通常是由于血源性播散而发展的,但目前尚不清楚循环中的阿米巴如何进入中枢神经系统 (CNS) 并引起炎症。目前,棘阿米巴用于入侵这个保护得非常好的中枢神经系统区域并产生感染的机制尚不清楚。在本文中,我们提出了两个关键的毒力因子:甘露糖结合蛋白和细胞外丝氨酸蛋白酶,它们是棘阿米巴穿透血脑屏障导致神经元损伤的关键因素。这两种分子都为合理开发针对棘阿米巴脑炎的治疗干预措施提供了极好的潜在靶点。