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Analysis of the presence of signals apoptotics, necrotics and/or NETose during incubation of human neutrophil with parasite Trypanosoma cruzi

Grant number: 12/23068-7
Support type:Scholarships in Brazil - Scientific Initiation
Effective date (Start): April 01, 2013
Effective date (End): December 31, 2013
Field of knowledge:Biological Sciences - Immunology - Cellular Immunology
Principal researcher:Karina Alves de Toledo
Grantee:Priscila Silva Sampaio de Souza
Home Institution: Faculdade de Ciências e Letras (FCL-ASSIS). Universidade Estadual Paulista (UNESP). Campus de Assis. Assis , SP, Brazil

Abstract

Diseases triggered by protozoa consist of serious public health problem, mainly due to the relative high rate of mortality associated with them. Chagas disease described for the first time in 1909 by Carlos Chagas and which etiologic agent is Trypanosoma cruzi, may present fatal events, including myocardial inflammation, meningeal and brain regions. Currently, control of replication of this parasite, aided or not by drug treatments, involves immune response intense and persistent and it included innate immunity cells such as monocytes, eosinophils and neutrophils. A new paradigm in innate immunity has recently been described in which neutrophils release their DNA in response to infectious stimuli. The NETs (neutrophil extracellular traps) quickly capture and kill several pathogens, including bacteria, fungi, and recently, parasites of Leishmania sp and Toxoplasma gondii, contributing to the control of replication and elimination of these microorganisms by the host. Quite interesting and intriguing, the process of formation of NETs, called NETose, is described by engaging pro-inflammatory immune response, antimicrobial and for present morphological and molecular signals distinct from those presented by the processes of apoptosis and necrosis. Preliminary results from our group suggest that incubation of human neutrophils with parasite T. cruzi stimulates formation of NETs. Thus, the central objective of this project is to investigate the induction of cell death in neutrophils during infection with T. cruzi and point if this occurs by apoptosis, necrosis or NETose, evaluating their distinctions. This project will assist in developing new strategies to control the inflammatory response during infection by T. cruzi in order to control the parasite load and therefore the pathogenesis associated with it.(AU)

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