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Silva-Neto MA, Carneiro AB, Silva-Cardoso L, et al. Lysophosphatidylcholine: A Novel Modulator of Trypanosoma cruzi Transmission. J Parasitol Res. 2011;2012:625838doi: 10.1155/2012/625838.
Silva-Neto, M. A., Carneiro, A. B., Silva-Cardoso, L., & Atella, G. C. (2012). Lysophosphatidylcholine: A Novel Modulator of Trypanosoma cruzi Transmission. Journal of parasitology research, 2012625838. https://doi.org/10.1155/2012/625838
Silva-Neto, Mário A C, et al. "Lysophosphatidylcholine: A Novel Modulator of Trypanosoma cruzi Transmission." Journal of parasitology research vol. 2012 (2012): 625838. doi: https://doi.org/10.1155/2012/625838
Silva-Neto MA, Carneiro AB, Silva-Cardoso L, Atella GC. Lysophosphatidylcholine: A Novel Modulator of Trypanosoma cruzi Transmission. J Parasitol Res. 2012;2012:625838. doi: 10.1155/2012/625838. Epub 2011 Nov 01. PMID: 22132309; PMCID: PMC3206328.
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J Parasitol Res. 2012;2012:625838. doi: 10.1155/2012/625838. Epub 2011 Nov 01.

Lysophosphatidylcholine: A Novel Modulator of Trypanosoma cruzi Transmission.

Journal of parasitology research

Mário A C Silva-Neto, Alan B Carneiro, Livia Silva-Cardoso, Georgia C Atella

Affiliations

  1. Instituto de Bioquímica Médica at Universidade Federal do Rio de Janeiro (UFRJ), 21940-590 Rio de Janeiro, RJ, Brazil.

PMID: 22132309 PMCID: PMC3206328 DOI: 10.1155/2012/625838

Abstract

Lysophosphatidylcholine is a bioactive lipid that regulates a large number of cellular processes and is especially present during the deposition and infiltration of inflammatory cells and deposition of atheromatous plaque. Such molecule is also present in saliva and feces of the hematophagous organism Rhodnius prolixus, a triatominae bug vector of Chagas disease. We have recently demonstrated that LPC is a modulator of Trypanosoma cruzi transmission. It acts as a powerful chemoattractant for inflammatory cells at the site of the insect bite, which will provide a concentrated population of cells available for parasite infection. Also, LPC increases macrophage intracellular calcium concentrations that ultimately enhance parasite invasion. Finally, LPC inhibits NO production by macrophages stimulated by live T. cruzi, and thus interferes with the immune system of the vertebrate host. In the present paper, we discuss the main signaling mechanisms that are likely used by such molecule and their eventual use as targets to block parasite transmission and the pathogenesis of Chagas disease.

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