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(Reference retrieved automatically from SciELO through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

The effects of nitric oxide on the immune system during Trypanosoma cruzi infection

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Author(s):
Fredy RS Gutierrez [1] ; Tiago WP Mineo [2] ; Wander R Pavanelli [3] ; Paulo MM Guedes [4] ; João S Silva [5]
Total Authors: 5
Affiliation:
[1] Universidade de São Paulo. Faculdade de Medicina de Ribeirão Preto. Departamento de Bioquímica e Imunologia - Brasil
[2] Universidade de São Paulo. Faculdade de Medicina de Ribeirão Preto. Departamento de Bioquímica e Imunologia - Brasil
[3] Universidade de São Paulo. Faculdade de Medicina de Ribeirão Preto. Departamento de Bioquímica e Imunologia - Brasil
[4] Universidade de São Paulo. Faculdade de Medicina de Ribeirão Preto. Departamento de Bioquímica e Imunologia - Brasil
[5] Universidade de São Paulo. Faculdade de Medicina de Ribeirão Preto. Departamento de Bioquímica e Imunologia - Brasil
Total Affiliations: 5
Document type: Journal article
Source: Memórias do Instituto Oswaldo Cruz; v. 104, p. 236-245, 2009-07-00.
Abstract

Trypanosoma cruzi infection triggers substantial production of nitric oxide (NO), which has been shown to have protective and toxic effects on the host's immune system. Sensing of trypomastigotes by phagocytes activates the inducible NO-synthase (NOS2) pathway, which produces NO and is largely responsible for macrophage-mediated killing of T. cruzi. NO is also responsible for modulating virtually all steps of innate and adaptive immunity. However, NO can also cause oxidative stress, which is especially damaging to the host due to increased tissue damage. The cytokines IFN-³ and TNF-±, as well as chemokines, are strong inducers of NOS2 and are produced in large amounts during T. cruzi acute infection. Conversely, TGF-² and IL-10 negatively regulate NO production. Here we discuss the recent evidence describing the mechanisms by which NO is able to exert its antimicrobial and immune regulatory effects, the mechanisms involved in the oxidative stress response during infection and the implications of NO for the development of therapeutic strategies against T. cruzi. (AU)

FAPESP's process: 07/04896-8 - Participation of IL-17 how molecular marker of clinical forms of Chagas' disease
Grantee:Paulo Marcos da Matta Guedes
Support Opportunities: Scholarships in Brazil - Post-Doctoral
FAPESP's process: 06/06803-4 - The role of Toll like receptors in the imune response towards Neospora caninum
Grantee:Tiago Wilson Patriarca Mineo
Support Opportunities: Scholarships in Brazil - Post-Doctoral
FAPESP's process: 07/53940-0 - The regulatory T cells and TH17 in the immune response against infections, tumors and autoimmune diseases
Grantee:João Santana da Silva
Support Opportunities: Research Projects - Thematic Grants