Glycosylation Patterns in Gut: Implications for the Development of Vector Control Strategies.

The primary mode of transmission for Chagas disease is vector-borne transmission, spread by hematophagous insects of the subfamily. In Mexico, the triatomine is particularly significant in the transmission of . This study focused on analyzing protein expression and modifications by glycosylation in different regions of the digestive tract of fifth-instar nymphs of .

Differential Regulation of L-Arginine Metabolism through NOS2 and Arginases during Infection with .

L-arginine metabolism through arginases and inducible nitric oxide synthase (NOS2) constitutes a fundamental axis for the resolution or progression of Chagas disease. Infection with can cause a wide spectrum of disease, ranging from acute forms contained by the host immune response to chronic ones, such as the chronic chagasic cardiomyopathy. Here, we analyzed, in an in vitro model, the ability of two isolates, with different degrees of virulence, to regulate the metabolism of L-arginine through arginase 1 (Arg-1) and NOS2 in macrophages and through arginase 2 (Arg-2) and NOS2 in cardiomyocytes.

Expression of Proteins, Glycoproteins, and Transcripts in the Guts of Fasting, Fed, and -Infected Triatomines: A Systematic Review.

Chagas disease is caused by the hemoflagellate protozoan 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 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.

Main Cardiac Histopathologic Alterations in the Acute Phase of Infection in a Murine Model.

Symptoms in the acute phase of Chagas disease are usually mild and nonspecific. However, after several years, severe complications like dilated heart failure and even death may arise in the chronic phase. Due to the lack of specific symptoms in the acute phase, the aim of this work was to describe and analyze the cardiac histopathology during this phase in a CD1 mouse model by assessing parasitism, fibrotic damage, and the presence and composition of a cellular infiltrate, to determine its involvement in the pathogenesis of lesions in the cardiac tissue.

Immunopathological Mechanisms Underlying Cardiac Damage in Chagas Disease.

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 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.