ArticleInfection and immunity2004
Inducible nitric oxide synthase is not essential for control of Trypanosoma cruzi infection in mice.
Article in Infection and immunity, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
27 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.
- Pooled it
- Animal models for exploring Chagas disease pathogenesis and supporting drug discovery.Clinical microbiology reviews · 2024Review
- Inflammation and mitochondria in the pathogenesis of chronic Chagas disease cardiomyopathy.Experimental biology and medicine (Maywood, N.J.) · 2023Review
- IFN-induced cell-autonomous immune mechanisms in the control of intracellular protozoa.Parasitology research · 2022Review
- Predicting Blood Parasite Load and Influence of Expression of iNOS on the Effect Size of Clinical Laboratory Parameters in AcuteFrontiers in immunology · 2022Article
- Modulation of STAT-1, STAT-3, and STAT-6 activities in THP-1 derived macrophages infected with twoFrontiers in immunology · 2022Article
- Sustained Inhibition of NF-κB Activity Mitigates Retinal Vasculopathy in Diabetes.The American journal of pathology · 2021Article
- Host-parasite dynamics in Chagas disease from systemic to hyper-local scales.Parasite immunology · 2021Review
- Genetic Ablation of the Inducible Form of Nitric Oxide in Male Mice Disrupts Immature Neuron Survival in the Adult Dentate Gyrus.Frontiers in immunology · 2021Article
- Myeloid-Derived Suppressor Cells inFrontiers in cellular and infection microbiology · 2021Review
- Differences in cNOS/iNOS Activity during Resistance to Trypanosoma cruzi Infection in 5-Lipoxygenase Knockout Mice.Mediators of inflammation · 2019Article
- Endogenous overexpression of an active phosphorylated form of DNA polymerase β under oxidative stress in Trypanosoma cruzi.PLoS neglected tropical diseases · 2018Article
- L-arginine supplementation reduces mortality and improves disease outcome in mice infected with Trypanosoma cruzi.PLoS neglected tropical diseases · 2018Article
- Article
- Disease Tolerance and Pathogen Resistance Genes May UnderlieFrontiers in immunology · 2018Article
- Role of Inactive and ActiveFrontiers in microbiology · 2017Article
- Sympathetic glial cells and macrophages develop different responses to Trypanosoma cruzi infection or lipopolysaccharide stimulation.Memorias do Instituto Oswaldo Cruz · 2014Article
- NADPH phagocyte oxidase knockout mice control Trypanosoma cruzi proliferation, but develop circulatory collapse and succumb to infection.PLoS neglected tropical diseases · 2012Article
- Pathogen-induced proapoptotic phenotype and high CD95 (Fas) expression accompany a suboptimal CD8+ T-cell response: reversal by adenoviral vaccine.PLoS pathogens · 2012Article
- 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
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Immune control of many intracellular pathogens, including Trypanosoma cruzi, is reported to be dependent on the production of nitric oxide. In this study, we show that mice deficient in inducible nitric oxide synthase (iNOS or NOS2) exhibit resistance to T. cruzi infection that is comparable to that of wild-type mice. This is the case for two iNOS-deficient mouse strains, Nos2(tm1Lau) and Nos2 N5, infected with the Brazil or Tulahuen strain of T. cruzi. In all cases, blood parasitemia, tissue parasite load, and survival rates are similar between wild-type and iNOS-deficient mice. In contrast, both wild-type and Nos2(tm1Lau) mice died within 32 days postinfection when treated with the nitric oxide synthase inhibitor aminoguanidine. Increased transcription of NOS1 or NOS3 is not found in iNOS-knockout (KO) mice, indicating that the absence of nitric oxide production through iNOS is not compensated for by increased production of other NOS isoforms. However, Nos2(tm1Lau) mice exhibit enhanced expression of tumor necrosis factor alpha, interleukin-1, and macrophage inflammatory protein 1alpha compared to that of wild-type mice, and these alterations may in part compensate for the lack of iNOS. These results clearly show that iNOS is not required for control of T. cruzi infection in mice.
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Registered trials
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