The aim of this study was to evaluate the activity of purinergic enzymes in lymphocytes and cardiac tissue of mice experimentally infected by Trypanosoma cruzi. Twelve female mice were used, divided into two groups (n = 6): uninfected and infected. On day 12 post-infection (PI), the animals were anesthetized and after euthanized, and samples were collected for analyses. Infected mice showed reduction in erythrocyte counts, hematocrit and hemoglobin concentration, as well as reduced number of total leukocytes in consequence of neutrophilia (P < 0.01). The number of monocytes increased in infected mice (P < 0.001), however the number of lymphocytes and eosinophils did not differ between groups (P > 0.05). The E-NTPDase (ATP and ADP substrate) and E-ADA activities in lymphocytes increased significantly in mice infected by T. cruzi (P < 0.01). In the heart, multiple pseudocysts containing amastigotes within cardiomyocytes were observed, as well as focally extensive severe necrosis associated with diffuse moderate to severe inflammatory infiltrate of lymphocytes. Although, the NTPDase activity (ATP and ADP substrate) in the cardiac homogenate did not differ between groups, a reduction on 5'-nucleotidase activity (P < 0.001) and an increase in the ADA activity in infected animals (P < 0.05) were observed. Thus, animals infected by T. cruzi experienced the disease, i.e., showed anemia, leucopenia, and heart lesions. Associated with this, purinergic enzymes showed altered activities, which might be related to the modulation of the inflammatory response.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/j.exppara.2017.02.002 | DOI Listing |
PLoS Negl Trop Dis
January 2025
Centro de Investigaciones Epidemiológica y Salud Pública (CIESP-IECS) CONICET.
Background: Trypanosoma cruzi is a protozoan parasite which causes Chagas disease. Mother-to-child transmission is the main route of transmission in vector-free areas. Congenital Chagas disease refers specifically to cases arising from this route of transmission.
View Article and Find Full Text PDFMicrobiol Spectr
January 2025
Department of Molecular and Comparative Pathobiology, Johns Hopkins University, School of Medicine, Baltimore, Maryland, USA.
Unlabelled: is a protozoan parasite that causes human and animal African trypanosomiases (HAT and AAT). Cardiac symptoms are commonly reported in HAT patients, and intracardiac parasites with accompanying myocarditis have been observed in both natural hosts and animal models of infection. Despite the importance of as a cause of cardiac dysfunction and the dramatic socioeconomic impact of African trypanosomiases in sub-Saharan Africa, there are currently no reproducible murine models of associated cardiomyopathy.
View Article and Find Full Text PDFActa Parasitol
January 2025
Edificio D, Facultad de Ciencias Químicas, LADISER Inmunología y Biología Molecular, Universidad Veracruzana, Orizaba, Veracruz, México.
Despite being the most relevant and critical option for managing Chagas disease, pharmacological therapy is currently limited by the availability of only two drugs, benznidazole and nifurtimox. Their effectiveness is further restricted in the chronic phase of the infection, as they induce severe side effects and require prolonged treatment. Additionally, the use of these drugs can lead to the emergence of substantial resistance problems, compounded by the potential natural resistance of some parasite isolates.
View Article and Find Full Text PDFJCI Insight
January 2025
Department of Tropical Medicine and Infectious Disease, Tulane University, New Orleans, United States of America.
Chagas disease is a neglected tropical disease caused by Trypanosoma cruzi with clinical presentations ranging from asymptomatic to cardiac and/or gastrointestinal complications. The mechanisms of pathogenesis are still poorly understood, but T. cruzi strain diversity may be associated with disease progression.
View Article and Find Full Text PDFClin Microbiol Rev
January 2025
School of Infection and Immunity, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, United Kingdom.
SUMMARYPrior to 2019, when the orally available drug fexinidazole began its clinical use, the treatment of human African trypanosomiasis (HAT) was complex and unsatisfactory for many reasons. Two sub-species of the parasite are responsible for HAT, namely the rhodesiense form found in East and Southern Africa and the gambiense form found in Central and West Africa. Diseases caused by both forms manifest in two stages: stage 1 before and stage 2 after central nervous system involvement.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!