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Differential expression profiles in the midgut of Triatoma infestans infected with Trypanosoma cruzi.

ABSTRACT: Chagas disease, or American trypanosomiasis, is a parasitic disease caused by the protozoan Trypanosoma cruzi and is transmitted by insects from the Triatominae subfamily. To identify components involved in the protozoan-vector relationship, we constructed and analyzed cDNA libraries from RNA isolated from the midguts of uninfected and T. cruzi-infected Triatoma infestans, which are major vectors of Chagas disease. We generated approximately 440 high-quality Expressed Sequence Tags (ESTs) from each T. infestans midgut cDNA library. The sequences were grouped in 380 clusters, representing an average length of 664.78 base pairs (bp). Many clusters were not classified functionally, representing unknown transcripts. Several transcripts involved in different processes (e.g., detoxification) showed differential expression in response to T. cruzi infection. Lysozyme, cathepsin D, a nitrophorin-like protein and a putative 14 kDa protein were significantly upregulated upon infection, whereas thioredoxin reductase was downregulated. In addition, we identified several transcripts related to metabolic processes or immunity with unchanged expressions, including infestin, lipocalins and defensins. We also detected ESTs encoding juvenile hormone binding protein (JHBP), which seems to be involved in insect development and could be a target in control strategies for the vector. This work demonstrates differential gene expression upon T. cruzi infection in the midgut of T. infestans. These data expand the current knowledge regarding vector-parasite interactions for Chagas disease.

SUBMITTER: Buarque DS

PROVIDER: S-EPMC3642171 | biostudies-literature | 2013

REPOSITORIES: biostudies-literature

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Differential expression profiles in the midgut of Triatoma infestans infected with Trypanosoma cruzi.

Buarque Diego S DS Braz Glória R C GR Martins Rafael M RM Tanaka-Azevedo Anita M AM Gomes Cícera M CM Oliveira Felipe A A FA Schenkman Sergio S Tanaka Aparecida S AS

PloS one 20130502 5

Chagas disease, or American trypanosomiasis, is a parasitic disease caused by the protozoan Trypanosoma cruzi and is transmitted by insects from the Triatominae subfamily. To identify components involved in the protozoan-vector relationship, we constructed and analyzed cDNA libraries from RNA isolated from the midguts of uninfected and T. cruzi-infected Triatoma infestans, which are major vectors of Chagas disease. We generated approximately 440 high-quality Expressed Sequence Tags (ESTs) from e ...[more]

PMID: 23658688

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Project description:BackgroundTrypanosoma cruzi, the agent of Chagas disease, is a protozoan parasite transmitted to humans by blood-sucking triatomine vectors. However, and despite its utmost biological and epidemiological relevance, T. cruzi development inside the digestive tract of the insect remains a poorly understood process.Methods/principle findingsHere we showed that Gp35/50 kDa mucins, the major surface glycoproteins from T. cruzi insect-dwelling forms, are involved in parasite attachment to the internal cuticle of the triatomine rectal ampoule, a critical step leading to its differentiation into mammal-infective forms. Experimental evidence supporting this conclusion could be summarized as follows: i) native and recombinant Gp35/50 kDa mucins directly interacted with hindgut tissues from Triatoma infestans, as assessed by indirect immunofluorescence assays; ii) transgenic epimastigotes over-expressing Gp35/50 kDa mucins on their surface coat exhibited improved attachment rates (~2-3 fold) to such tissues as compared to appropriate transgenic controls and/or wild-type counterparts; and iii) certain chemically synthesized compounds derived from Gp35/50 kDa mucins were able to specifically interfere with epimastigote attachment to the inner lining of T. infestans rectal ampoules in ex vivo binding assays, most likely by competing with or directly blocking insect receptor(s). A solvent-exposed peptide (smugS peptide) from the Gp35/50 kDa mucins protein scaffolds and a branched, Galf-containing trisaccharide (Galfβ1-4[Galpβ1-6]GlcNAcα) from their O-linked glycans were identified as main adhesion determinants for these molecules. Interestingly, exogenous addition of a synthetic Galfβ1-4[Galpβ1-6]GlcNAcα derivative or of oligosaccharides containing this structure impaired the attachment of Dm28c but not of CL Brener epimastigotes to triatomine hindgut tissues; which correlates with the presence of Galf residues on the Gp35/50 kDa mucins' O-glycans on the former but not the latter parasite clone.Conclusion/significanceThese results provide novel insights into the mechanisms underlying T. cruzi-triatomine interplay, and indicate that inter-strain variations in the O-glycosylation of Gp35/50 kDa mucins may lead to differences in parasite differentiation and hence, in parasite transmissibility to the mammalian host. Most importantly, our findings point to Gp35/50 kDa mucins and/or the Galf biosynthetic pathway, which is absent in mammals and insects, as appealing targets for the development of T. cruzi transmission-blocking strategies.

Project description:BackgroundTriatomine elimination efforts and the interruption of domestic transmission of Trypanosoma cruzi are hampered by pyrethroid resistance. Fluralaner, a long-lasting ectoparasiticide administered to dogs, substantially reduced site infestation and abundance of pyrethroid-resistant Triatoma infestans Klug (Heteroptera: Reduviidae) in an ongoing 10-month trial in Castelli (Chaco Province, Argentina). We assessed the effects of fluralaner on vector infection with T. cruzi and blood meal sources stratified by ecotope and quantified its medium-term effects on site infestation and triatomine abundance.MethodsWe conducted a placebo-controlled, before-and-after efficacy trial of fluralaner in 28 infested sites over a 22-month period. All dogs received either an oral dose of fluralaner (treated group) or placebo (control group) at 0 month post-treatment [MPT]. Placebo-treated dogs were rescue-treated with fluralaner at 1 MPT, as were all eligible dogs at 7 MPT. Site-level infestation and abundance were periodically assessed by timed manual searches with a dislodging aerosol. Vector infection was mainly determined by kDNA-PCR and blood meal sources were determined by enzyme-linked immunosorbent assay.ResultsIn fluralaner-treated households, site infestation dropped from 100% at 0 MPT to 18-19% over the period 6-22 MPT while mean abundance plummeted from 5.5 to 0.6 triatomines per unit effort. In control households, infestation dropped similarly post-treatment. The overall prevalence of T. cruzi infection steadily decreased from 13.8% at 0-1 MPT (baseline) to 6.4% and subsequently 2.3% thereafter, while in domiciles, kitchens and storerooms it dropped from 17.4% to 4.7% and subsequently 3.3% thereafter. Most infected triatomines occurred in domiciles and had fed on humans. Infected-bug abundance plummeted after fluralaner treatment and remained marginal or nil thereafter. The human blood index of triatomines collected in domiciles, kitchens and storerooms highly significantly fell from 42.9% at baseline to 5.3-9.1% over the period 6-10 MPT, increasing to 36.8% at 22 MPT. Dog blood meals occurred before fluralaner administration only. The cat blood index increased from 9.9% at baseline to 57.9-72.7% over the period 6-10 MPT and dropped to 5.3% at 22 MPT, whereas chicken blood meals rose from 39.6% to 63.2-88.6%.ConclusionFluralaner severely impacted infestation- and transmission-related indices over nearly 2 years, causing evident effects at 1 MPT, and deserves larger efficacy trials.

Dataset Information

Differential expression profiles in the midgut of Triatoma infestans infected with Trypanosoma cruzi.

Publications

Differential expression profiles in the midgut of Triatoma infestans infected with Trypanosoma cruzi.

Similar Datasets

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