Galectin-3 mediates survival and apoptosis pathways during Trypanosoma cruzi-host cell interplay.

Galectin-3 mediates survival and apoptosis pathways during Trypanosoma cruzi-host cell interplay. Exp Parasitol. 2020 Jun 11;:107932 Authors: de Oliveira Chain M, Augusto de Medeiros Paiva C, de Oliveira Maciel I, Neto AN, Castro VF, Oliveira CP, Mendonça BDS, Nestal de Moraes G, Albert Dos Reis S, Alex de Carvalho M, Barbosa De-Melo LD Abstract Neglected tropical diseases, such as Chagas disease caused by the protozoa Trypanosoma cruzi, affect millions of people worldwide but lack effective treatments that are accessible to the entire population, especially patients with the debilitating chronic phase. The recognition of host cells, invasion and its intracellular replicative success are essential stages for progression of the parasite life cycle and the development of Chagas disease. It is predicted that programmed cell death pathways (apoptosis) would be activated in infected cells, either via autocrine secretion or mediated by cytotoxic immune cells. This process should play a key role in resolving infections by hindering the evolutionary success of the parasite. In this research, we performed assays to investigate the role of the lectin galectin-3 (Gal3) in parasite-host signaling pathways. Using cells with endogenous levels of Gal3 compared to Gal3-deficient cells (induced by RNA interference), we demonstrated that T. cruzi mediated the survival pathways and the subverted apoptosis through Gal3 promoting a pro-survival state in...
Source: Experimental Parasitology - Category: Parasitology Authors: Tags: Exp Parasitol Source Type: research