Evaluation of macrophage activation and identification of cell death during in vitro infection with different isolates from Paracoccidioides spp. genus

• Grant number: 16/08667-2
• Support Opportunities: Scholarships in Brazil - Scientific Initiation
• Start date: August 01, 2016
• End date: July 31, 2017
• Field of knowledge: Biological Sciences - Microbiology - Biology and Physiology of Microorganisms
• Principal Investigator: Ana Camila Oliveira Souza
• Grantee: Abigail Mirela Gouveia
• Host Institution: Instituto de Ciências Biomédicas (ICB). Universidade de São Paulo (USP). São Paulo , SP, Brazil

Abstract

Paracoccidioidomycosis (PCM) is a deep mycosis endemic in Latin America caused by thermodimorphic fungi of the genus Paracoccidioides spp. Phagocytic cells have fundamental importance for the protection of the host against these pathogens, producing anti-microbial substances and pro-inflammatory molecules, and promoting the development of innate immunity. However, these fungi have the potential to survive within macrophages, invade other tissues and persist in the host. Infected macrophages cell death is an important factor in the evolution of infectious diseases and may lead to protection of host cells and removal of intracellular microbial niche, exposing it to the extracellular medium. On the other hand, some pathogens induce host cell death to evade immune cell activity and persist in the host. Some studies have shown the induction of cell death by P. brasiliensis infected peritoneal and epithelial cells and even apoptosis, relating it to disease resistance. However, there are no reports on the influence of P. lutzii infection in host cell death and its consequences in the pathogenesis of PCM. Considering the need for further studies to compare pathogenic differences among isolates of each species of the genus Paracoccidioides spp., this work aims to evaluate the activation of macrophages and identify the occurrence of cell death during the interaction in vitro with P. brasiliensis and P. lutzii isolates.