Zinc: phenotypic characterization of T lymphocytes, and Treg cells during pregnancy in wistar rats infected with the Y strain Trypanosoma cruzi

Abstract

Chagas disease is one of the most serious parasitic diseases in Latin America. Currently, between 6 and 7 million people are infected, and about 40 million are at risk of becoming infected. The problem is congenital Chagas infection in endemic and non-endemic areas, may cause miscarriage, prematurity, growth retardation intrauterine placentitis, Intrauterine and neonatal death. Interaction between the membrane receptor of T lymphocytes (TCR) with peptide complex- MHC is essential for T-lymphocyte activation and differentiation into effector and memory cells. During pregnancy, immunological and physiological adjustments occur in the mother that ensures the success or failure of pregnancy. Although the mechanisms for generation and maintenance of memory T cells are not yet fully understood, the importance of these cells for the immune response arises from the fact that they persist long prolongado.Sabe that proinflammatory cytokines such as IL-1, IL -6 and TNF-³ activate the hypothalamic-pituitary-adrenal (HPA) axis, resulting in increased production of glucocorticoids in the circulation (corticosterone in rodents and cortisol in humans). The severe depletion of cortical thymocytes via apoptosis, most CD4 + CD8 + that occurs during the acute phase of infection with T. cruzi is mediated directly by glucocorticoids and TNF-± is involved in the release of this hormone during illness. developed due to immunosuppression during pregnancy, with the induction of Th2 response by CD4 + T cells can occur reactivation of Chagas disease mothers. Thus, pregnant women presenting to the indeterminate or chronic disease may re-develop acute symptoms such as high parasitemia and serum IgM, further contributing to the occurrence of transplacental transmission of the parasite. Zinc deficiency observed in pregnant women and newborns in developed and developing countries, can alter fetal development and postnatal. Previous studies show that severe zinc deficiency causes growth retardation in rats. Given the results obtained in our laboratory demonstrated that administration of zinc sulfate reduces parasitemia in pregnant rats infected with the Y strain of T. cruzi, the goal of this research is to perform phenotypic characterization of T cells, and Treg cells, as well as assessment of cell apoptosis during pregnancy in Wistar rats infected with T. cruzi and are supplemented with zinc sulphate. (AU)