IAI Accepts, published online ahead of print on 15 September 2008

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Infect. Immun. doi:10.1128/IAI.00683-08
Copyright (c) 2008, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Trypanosoma cruzi infection is enhanced by vector saliva through immunosuppressant mechanisms mediated by lysophosphatidylcholine

Rafael D. Mesquita, Alan Brito Carneiro, André Bafica, Felipe Gazos-Lopes, Christina M. Takiya, Thaís Souto-Padron, Danielle P. Vieira, Antônio Ferreira-Pereira, Igor C. Almeida, Rodrigo T. Figueiredo, Bárbara N. Porto, Marcelo T. Bozza, Aurélio Graça-Souza, Angela H. C. S. Lopes, Geórgia C. Atella, and Mário A. C. Silva-Neto^*

From the Instituto de Bioquímica Médica, Instituto de Ciências Biomédicas, Departamento de Histologia e Embriologia, and Instituto de Microbiologia Professor Paulo de Góes at Universidade Federal do Rio de Janeiro, UFRJ, 21940-590, Rio de Janeiro, RJ, Brazil; Divisão de Imunologia, Departamento de Microbiologia e Parasitologia, Universidade Federal de Santa Catarina, 88040-900, Florianópolis, SC, Brasil; Department of Biological Sciences, The Border Biomedical Research Center, University of Texas at El Paso, El Paso, TX 79968, USA

^* To whom correspondence should be addressed. Email: maneto{at}bioqmed.ufrj.br.

Trypanosoma cruzi, the etiological agent of Chagas disease, is transmitted by bug feces deposited on human skin during a blood meal. However, parasite infection occurs through the wound produced by insect mouthparts. Saliva of the triatominae bug Rhodnius prolixus is a source of lysophosphatidylcholine (LPC). Here, we tested the role of both triatomine saliva and LPC on parasite transmission. We show that vector saliva is a powerful inducer of cell chemotaxis. A massive number of inflammatory cells were found at the sites where LPC or saliva was inoculated into the mouse skin. LPC is a known chemoattractant for monocytes but neutrophil recruitment induced by saliva is LPC-independent. Pre-incubation of peritoneal macrophages with saliva or LPC increased five-fold the association of T. cruzi with these cells. Moreover, saliva and LPC block nitric oxide production by T. cruzi-exposed macrophages. Injection of saliva or LPC into mouse skin in the presence of the parasite induces an up to six-fold increase in blood parasitemia. Together, our data suggest that triatominae saliva enhance T. cruzi transmission and some of its biological effects are attributed to LPC. This is a demonstration that a vector-derived lysophospholipid may act as an enhancing factor of Chagas disease.