The Effects of Nitric Oxide on the Immune System During Trypanosoma Cruzi Infection
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...
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Published in | Memórias do Instituto Oswaldo Cruz Vol. 104; no. s1; pp. 236 - 245 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English Portuguese |
Published |
Brazil
Fundação Oswaldo Cruz, Fiocruz
01.07.2009
Instituto Oswaldo Cruz, Ministério da Saúde Fundação Oswaldo Cruz (FIOCRUZ) |
Subjects | |
Online Access | Get full text |
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Summary: | 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-γ and TNF-α, as well as
chemokines, are strong inducers of NOS2 and are produced in large
amounts during T. cruzi acute infection. Conversely, TGF-β 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. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 1678-8060 0074-0276 1678-8060 0074-0276 |
DOI: | 10.1590/s0074-02762009000900030 |