Abstract
Background TcSMUG L products were recently identified as novel mucin-type glycoconjugates restricted to the surface of insect-dwelling epimastigote forms of Trypanosoma cruzi, the etiological agent of Chagas disease. The remarkable conservation of their predicted mature N-terminal region, which is exposed to the extracellular milieu, suggests that TcSMUG L products may be involved in structural and/or functional aspects of the interaction with the insect vector.Methodology and Principal FindingsHere, we investigated the putative roles of TcSMUG L mucins in both in vivo development and ex vivo attachment of epimastigotes to the luminal surface of the digestive tract of Rhodnius prolixus. Our results indicate that the exogenous addition of TcSMUG L N-terminal peptide, but not control T. cruzi mucin peptides, to the infected bloodmeal inhibited the development of parasites in R. prolixus in a dose-dependent manner. Pre-incubation of insect midguts with the TcSMUG L peptide impaired the ex vivo attachment of epimastigotes to the luminal surface epithelium, likely by competing out TcSMUG L binding sites on the luminal surface of the posterior midgut, as revealed by fluorescence microscopy.Conclusion and SignificanceTogether, these observations indicate that TcSMUG L mucins are a determinant of both adhesion of T. cruzi epimastigotes to the posterior midgut epithelial cells of the triatomine, and the infection of the insect vector, R. prolixus.
Highlights
Described by its discoverer, Carlos Chagas [1,2], as ‘‘one of the most injurious tropical illnesses, specially to children in contaminated areas, either in determining a chronic sickly condition in which people become unable to perform vital activities or as an important factor of human degeneration,’’ Chagas disease remains a major tropical human disease in much of Latin America, affecting approximately 11 million people
Together, these observations indicate that TcSMUG L mucins are a determinant of both adhesion of T. cruzi epimastigotes to the posterior midgut epithelial cells of the triatomine, and the infection of the insect vector, R. prolixus
We investigated the role of TcSMUG L mucins in the attachment of T. cruzi epimastigotes from the Dm28c stock to the midgut epithelium of R. prolixus and the consequent development of the protozoan in the insect vector
Summary
Carlos Chagas [1,2], as ‘‘one of the most injurious tropical illnesses, specially to children in contaminated areas, either in determining a chronic sickly condition in which people become unable to perform vital activities or as an important factor of human degeneration,’’ Chagas disease remains a major tropical human disease in much of Latin America, affecting approximately 11 million people. Various triatomine vectors, including Rhodnius, Triatoma and Pastrongylus, are able to acquire and transmit Trypanosoma cruzi, the etiological agent of Chagas disease [4,5]. During their development within insects, parasites undergo profound morphological changes, modulating surface molecules to enable interactions with specific insect tissues that are essential for their survival, development and successful transmission to a vertebrate host [6,7]. Most of the bloodstream trypomastigotes differentiate into non-infective epimastigote forms. TcSMUG L products were recently identified as novel mucin-type glycoconjugates restricted to the surface of insect-dwelling epimastigote forms of Trypanosoma cruzi, the etiological agent of Chagas disease. The remarkable conservation of their predicted mature N-terminal region, which is exposed to the extracellular milieu, suggests that TcSMUG L products may be involved in structural and/or functional aspects of the interaction with the insect vector
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