Damatta Renato A, Seabra Sergio H, Deolindo Poliana, Arnholdt Andréa C V, Manhães Lauro, Goldenberg Samuel, de Souza Wanderley
Laboratório de Biologia Celular e Tecidual, Universidade Federal do Rio de Janeiro, Rio de Janerio, RJ, Brazil.
FEMS Microbiol Lett. 2007 Jan;266(1):29-33. doi: 10.1111/j.1574-6968.2006.00495.x. Epub 2006 Nov 1.
Chagas disease is caused by Trypanosoma cruzi and affects 18 million people in Central and South America. Here we analyzed the exposure of phosphatidylserine by the different forms of the parasite life cycle. Only the infective trypomastigotes, but not the epimastigotes or intracellular amastigotes, expose this phospholipid. This triggers a transforming growth factor beta signaling pathway, based on phosphorylated Smad 2 nuclear translocation, leading to iNOS disappearance in infected macrophages. This macrophage deactivation favors the survival of this intracellular parasite. Thus, phosphatidylserine exposure may be used by T. cruzi to evade innate immunity and be a common feature of obligate intracellular parasites that have to deal with activated macrophages.
恰加斯病由克氏锥虫引起，影响中南美洲1800万人。在此，我们分析了寄生虫不同生命周期形式下磷脂酰丝氨酸的暴露情况。只有感染性锥鞭毛体，而非无鞭毛体或细胞内无鞭毛体，会暴露这种磷脂。这会触发基于磷酸化Smad 2核转位的转化生长因子β信号通路，导致感染巨噬细胞中诱导型一氧化氮合酶消失。这种巨噬细胞失活有利于这种细胞内寄生虫的存活。因此，磷脂酰丝氨酸暴露可能被克氏锥虫用于逃避先天免疫，并且是必须应对活化巨噬细胞的专性细胞内寄生虫的共同特征。
