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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 Findings  Here, 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 Significance  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 .

Trypanosoma cruzi TcSMUG L-surface Mucins Promote Development and Infectivity in the Triatomine Vector Rhodnius prolixus