Open AccessTrypanosoma cruzi exposes phosphatidylserine as an evasion mechanism
Author(s) -
DaMatta Renato A.,
Seabra Sergio H.,
Deolindo Poliana,
Arnholdt Andréa C. V.,
Manhães Lauro,
Goldenberg Samuel,
De Souza Wanderley
Publication year - 2007
Publication title -
fems microbiology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.899
H-Index - 151
eISSN - 1574-6968
pISSN - 0378-1097
DOI - 10.1111/j.1574-6968.2006.00495.x
Subject(s) - trypanosoma cruzi , intracellular parasite , phosphatidylserine , intracellular , biology , microbiology and biotechnology , amastigote , macrophage , chagas disease , innate immune system , leishmania , parasite hosting , immune system , phospholipid , immunology , biochemistry , in vitro , membrane , world wide web , computer science
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.