Abstract
Trypanosoma cruzi is the causative agent of Chagas disease, a vector-borne disease. The parasite molecules involved in vector interaction have been little investigated. Metallopeptidases and gp63 molecules have been implicated in parasite adhesion of several trypanosomatids to the insect midgut. Although gp63 homologues are highly expanded in the T. cruzi genome, and are implicated in parasite-mammalian host interaction, its role in the insect vector has never been explored. Here, we showed that divalent metal chelators or anti-Tcgp63-I antibodies impaired T. cruzi adhesion to Rhodnius prolixus midgut. Parasites isolated after insect colonization presented a drastic enhancement in the expression of Tcgp63-I. These data highlight, for the first time, that Tcgp63-I and Zn-dependent enzymes contribute to the interaction of T. cruzi with the insect vector.
Highlights
Trypanosoma cruzi is the aetiological agent of Chagas disease, a vector-borne disease transmitted by the bite of a triatomine bug, which affects 8 million people worldwide (Perez-Molina and Molina, 2018)
Considering the structural similarities between T. cruzi and leishmanial gp63 molecules (El-Sayed and Donelson, 1997; Kulkarni et al, 2009; Abad-Franch et al, 2013), we evaluated the dose-dependent effect of phenanthroline on the proportion of parasite adhesion to the midgut
In phenanthroline doses ranging from 0.2 to 0.5 μM, the adhesion of epimastigotes was reduced in the range of 39–83% in relation to the control (Fig. 2A), which supports the hypothesis that metallo-dependent enzymes play a role in the adhesion to R. prolixus
Summary
Trypanosoma cruzi is the aetiological agent of Chagas disease, a vector-borne disease transmitted by the bite of a triatomine bug, which affects 8 million people worldwide (Perez-Molina and Molina, 2018). Other triatomine species are known to transmit T. cruzi (Noireau et al, 2009; Bern et al, 2011; Waleckx et al, 2015), and several others are on the merge of becoming competent vectors, to sum up, vector domiciliation is an emerging threat (Salazar et al, 2015). Few studies have been performed on the characterization of T. cruzi molecules involved in the parasite adhesion, interaction and colonization of the insect. Glycoinositolphospholipids (GIPLs) are the major molecules expressed on the epimastigote cell surface. These molecules are involved in the parasite adhesion to the luminal surface of the insect midgut and may be one of the determinants of the infection in the vector (Nogueira et al, 2007). Gp72, cruzipain and calpain-like molecules may be involved in this part of the parasite life cycle (de Jesus et al, 1993; Basombrio et al, 2002; Ennes-Vidal et al, 2011; Uehara et al, 2012)
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