In Chagas disease, the mechanisms involved in cardiac damage are an active field of study. The factors underlying the evolution of lesions following infection by Trypanosoma cruzi and, in some cases, the persistence of its antigens and the host response, with the ensuing development of clinically observable cardiac damage, are analyzed in this review.

Chagas disease is caused by the hemoflagellate protozoan Trypanosoma cruzi. The main transmission mechanism for the parasite in endemic areas is contact with the feces of an infected triatomine bug. Part of the life cycle of T. cruzi occurs in the digestive tract of triatomines, where vector and parasite engage in a close interaction at a proteomic–molecular level. This interaction triggers replication and differentiation processes in the parasite that can affect its infectivity for the vertebrate host. With the aim of compiling and analyzing information from indexed publications on transcripts, proteins, and glycoproteins in the guts of fasting, fed, and T. cruzi-infected triatomines in the period 2000–2022, a systematic review was conducted following the PRISMA guidelines. Fifty-five original research articles retrieved from PubMed and ScienceDirect were selected; forty-four papers reported 1–26,946 transcripts, and twenty-one studies described 1–2603 peptides/proteins.

The primary mode of transmission for Chagas disease is vector-borne transmission, spread by hematophagous insects of the Triatominae subfamily. In Mexico, the triatomine Meccus pallidipennis is particularly significant in the transmission of Trypanosoma cruzi. This study focused on analyzing protein expression and modifications by glycosylation in different regions of the digestive tract of fifth-instar nymphs of M. pallidipennis. Two gut sections were dissected and extracted: the anterior midgut (AMG) and the proctodeum or rectum (RE). Proteins were extracted from each tissue sample and profiled by one- and two-dimensional electrophoresis; protein glycosylation was analyzed by lectin affinity. Our results showed significant differences in protein expression and glycosylation between both gut regions, with modifications being more frequent in the RE. The proteins HSP70, actin, and tubulin were analyzed, finding a differential expression of the latter two between AMG and RE. Understanding glycosylation patterns provides critical insights into vector–pathogen interactions that could eventually inform novel control approaches. Furthermore, the potential use of lectins as insecticidal agents highlights the broader implications of glycoprotein research in the future development of strategies on vector control to disrupt T. cruzi transmission.

The successful transmission of Trypanosoma cruzi, the causative agent of Chagas disease, depends on intricate interactions with its insect vector. In Mexico, Meccus pallidipennis is a relevant triatomine species involved in the parasite’s life cycle. In the gut of these insects, the parasite moves from the anterior midgut (AMG) to the posterior midgut (PMG), where it multiplies. Finally, T. cruzi differentiates into its infective form by metacyclogenesis in the proctodeum or rectum (RE). This study aimed to characterize and compare the protein and glycoprotein profiles of the anterior midgut (AMG) and rectum (RE) of M. pallidipennis, and to assess their potential association with T. cruzi metacyclogenesis, with special attention to sex-specific differences. Insects were infected with the T. cruzi isolate ITRI/MX/12/MOR (Morelos). Protein profiles were analyzed by polyacrylamide gel electrophoresis, while glycoproteins were detected using ConA, WGA, and PNA lectins. The metacyclogenesis index was calculated for male and female triatomines. A lower overlap of protein fractions was found in the RE compared to the AMG between sexes, suggesting functional sexual dimorphism. Infected females showed greater diversity in glycoprotein patterns in the RE, potentially related to higher blood intake and parasite burden. The metacyclogenesis index was significantly higher in females than in males. These findings highlight sex-dependent differences in gut protein and glycoprotein profiles in M. pallidipennis, which may influence the efficiency of T. cruzi development within the vector. Further proteomic studies are needed to identify the molecular components involved and clarify their roles in parasite differentiation and suggest new targets for disrupting parasite transmission within the vector.

Food deprivation induces intestinal adaptations in Triatoma pallidipennis, a hematophagous insect with intermittent feeding habits. The ability to survive long periods without food promotes the persistence of this vector in the environment and contributes to its evolutionary success. This study employed one- and two-dimensional electrophoretic techniques combined with Western blot to evaluate the abundance of α-tubulin, β-actin, and the heat shock protein HSP70. These proteins were more abundant in the anterior midgut tissue of unfed insects than in that of fed insects. As these responses were similar in females and males, the observed adaptations primarily depend on feeding status and intestinal region. These findings provide further insight into the intestinal physiology of T. pallidipennis, a vector of the flagellate parasite Trypanosoma cruzi, the causative agent of Chagas disease.