ArticleInfection and immunity2001
Stage-dependent role of nitric oxide in control of Trypanosoma cruzi infection.
Article in Infection and immunity, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 75 citations in OpenAlex.
- IL-33/ST2 Signaling Protects the Heart by Restraining Inflammation and Parasite Burden duringACS infectious diseases · 2026Article
- Dual and Opposite Roles of Reactive Oxygen Species (ROS) in Chagas Disease: Beneficial on the Pathogen and Harmful on the Host.Oxidative medicine and cellular longevity · 2020Review
- Potential Role of Antioxidants as Adjunctive Therapy in Chagas Disease.Oxidative medicine and cellular longevity · 2020Review
- Article
- The value of Nigella sativa in the treatment of experimentally induced rhinosinusitis.Acta otorhinolaryngologica Italica : organo ufficiale della Societa italiana di otorinolaringologia e chirurgia cervico-facciale · 2017Article
- Proline modulates the Trypanosoma cruzi resistance to reactive oxygen species and drugs through a novel D, L-proline transporter.PloS one · 2014Article
- NLRP3 controls Trypanosoma cruzi infection through a caspase-1-dependent IL-1R-independent NO production.PLoS neglected tropical diseases · 2013Article
- Inducible nitric oxide synthase in heart tissue and nitric oxide in serum of Trypanosoma cruzi-infected rhesus monkeys: association with heart injury.PLoS neglected tropical diseases · 2012Article
- Chemoprevention of Colon Cancer by iNOS-Selective Inhibitors.Forum on immunopathological diseases and therapeutics · 2012Article
- NADPH phagocyte oxidase knockout mice control Trypanosoma cruzi proliferation, but develop circulatory collapse and succumb to infection.PLoS neglected tropical diseases · 2012Article
- Distinct roles for nitric oxide in resistant C57BL/6 and susceptible BALB/c mice to control Burkholderia pseudomallei infection.BMC immunology · 2011Article
- Impaired innate immunity in Tlr4(-/-) mice but preserved CD8+ T cell responses against Trypanosoma cruzi in Tlr4-, Tlr2-, Tlr9- or Myd88-deficient mice.PLoS pathogens · 2010Article
- Perforin-expressing cytotoxic cells contribute to chronic cardiomyopathy in Trypanosoma cruzi infection.International journal of experimental pathology · 2010Article
- Cyclic AMP decreases the production of NO and CCL2 by macrophages stimulated with Trypanosoma cruzi GPI-mucins.Parasitology research · 2009Article
- Does cyclophosphamide play a protective role against neuronal loss in chronic T. cruzi infection?Digestive diseases and sciences · 2008Article
- Interaction of natural killer cells with Trypanosoma cruzi-infected fibroblasts.Clinical and experimental immunology · 2006Article
- High levels of interleukin-10 impair resistance to pulmonary coccidioidomycosis in mice in part through control of nitric oxide synthase 2 expression.Infection and immunity · 2006Article
- NK cells contribute to the control of Trypanosoma cruzi infection by killing free parasites by perforin-independent mechanisms.Infection and immunity · 2004Article
- Inducible nitric oxide synthase is not essential for control of Trypanosoma cruzi infection in mice.Infection and immunity · 2004Article
- Interferon-gamma-induced nitric oxide causes intrinsic intestinal denervation in Trypanosoma cruzi-infected mice.The American journal of pathology · 2004Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Trypanosoma cruzi, the causative agent of Chagas' disease, is known to be susceptible to nitric oxide (NO)-dependent killing by gamma interferon-activated macrophages. Mice deficient for inducible nitric oxide synthase (iNOS) are highly susceptible to T. cruzi, and inhibition of iNOS from the beginning of infection was reported to lead to an increase in trypomastigotes in the blood and to high mortality. In the present study, we investigated whether NO production is essential for the control of T. cruzi in all phases of the infection. BALB/c mice were treated at different time intervals after T. cruzi infection with an iNOS inhibitor, aminoguanidine or L-N6-(1-iminoethyl)-lysine (L-NIL). Treatment initiated with the beginning of the infection resulted in 100% mortality by day 16 postinfection (p.i.). If treatment was started later during the acute phase at the peak of parasitemia (day 20 p.i.), all the mice survived. Parasitemia was cleared and tissue amastigotes became undetectable in these mice even in the presence of the iNOS inhibitor L-NIL. Inhibition of iNOS in the chronic phase of the infection, i.e., from day 60 to day 120 p.i., with L-NIL did not result in a reappearance of parasitemia. These data suggest that while NO is essential for T. cruzi control in the early phase of acute infection, it is dispensable in the late acute and chronic phase, revealing a fundamental difference in control mechanisms compared to those in infections by other members of the order Kinetoplastida, e.g., Leishmania major.
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