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The role of nitric oxide in the pathogenesis of Chagas disease

Joao S Silva1, Fabiana S Machado, Gislaine A Martins

  • 1Department of Biochemistry and Immunology, School of Medicine of Ribeirão Preto-USP and Institute of Bimedical Sciences ICB-IV-USP 05508-900 São Paulo, SP, Brazil. jsdsilva@fmrp.usp.br

Frontiers in Bioscience : a Journal and Virtual Library
|July 25, 2003
PubMed

Insights

Nitric oxide (NO) production by inducible NO synthase (iNOS) aids in killing Trypanosoma cruzi but can also suppress immune responses and cause organ damage. This highlights NO

Area of Science:

  • Immunology
  • Parasitology
  • Molecular Biology

Background:

  • Infection with Trypanosoma cruzi presents complex immune responses.
  • Nitric oxide (NO) plays a dual role, exhibiting both protective and toxic effects.

Purpose of the Study:

  • To summarize the protective and toxic effects of nitric oxide (NO) during Trypanosoma cruzi infection.
  • To elucidate the role of inducible NO synthase (iNOS) in parasite killing and pathogenesis.

Main Methods:

  • Review of existing literature on NO production and its regulation during T. cruzi infection.
  • Analysis of the roles of cytokines (IFN-gamma, TNF-alpha, TGF-beta, IL-10) and chemoattractants.
  • Examination of iNOS expression in macrophages and cardiac tissues.

Main Results:

  • NO production, catalyzed by iNOS, is crucial for killing trypomastigotes.
  • Cytokines like IFN-gamma and TNF-alpha induce iNOS and NO-dependent parasite killing.
  • Negative regulators TGF-beta and IL-10 suppress NO production.
  • NO can suppress T cell-mediated immunity via apoptosis and is linked to cardiac dysfunction.

Conclusions:

  • The iNOS/NO pathway is a critical factor in controlling T. cruzi infection.
  • NO exhibits detrimental effects, including immune suppression and contribution to neuronal and myocardial dysfunction.
  • Understanding the dual role of NO is vital for developing therapeutic strategies against Chagas disease.

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