ArticlePLoS neglected tropical diseases2012
NADPH phagocyte oxidase knockout mice control Trypanosoma cruzi proliferation, but develop circulatory collapse and succumb to infection.
Article in PLoS neglected tropical diseases, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- Neutrophils versus Protozoan Parasites:Microorganisms · 2024Review
- Impact of IFN-γ Deficiency on the Cardiomyocyte Function in the First Stage of Experimental Chagas Disease.Microorganisms · 2022Article
- Myeloid-Derived Suppressor Cells inFrontiers in cellular and infection microbiology · 2021Review
- Reactive oxygen species and nitric oxide imbalances lead to in vivo and in vitro arrhythmogenic phenotype in acute phase of experimental Chagas disease.PLoS pathogens · 2020Article
- Metabolic syndrome agravates cardiovascular, oxidative and inflammatory dysfunction during the acute phase of Trypanosoma cruzi infection in mice.Scientific reports · 2019Article
- Reactive species and pathogen antioxidant networks during phagocytosis.The Journal of experimental medicine · 2019Review
- ROS and Trypanosoma cruzi: Fuel to infection, poison to the heart.PLoS pathogens · 2018Review
- Pathogenesis of Chronic Chagas Disease: Macrophages, Mitochondria, and Oxidative Stress.Current clinical microbiology reports · 2018Article
- Pentose Phosphate Shunt Modulates Reactive Oxygen Species and Nitric Oxide Production ControllingFrontiers in immunology · 2018Article
- Moderate Treadmill Exercise Training Improves Cardiovascular and Nitrergic Response and Resistance toFrontiers in physiology · 2017Article
- Trypanosoma cruzi Needs a Signal Provided by Reactive Oxygen Species to Infect Macrophages.PLoS neglected tropical diseases · 2016Article
- P47phox-/- mice are compromised in expansion and activation of CD8+ T cells and susceptible to Trypanosoma cruzi infection.PLoS pathogens · 2014Article
- Are reactive oxygen species always detrimental to pathogens?Antioxidants & redox signaling · 2014Review
- MnSODtg mice control myocardial inflammatory and oxidative stress and remodeling responses elicited in chronic Chagas disease.Journal of the American Heart Association · 2013Article
- Evolutionary dynamics of the human NADPH oxidase genes CYBB, CYBA, NCF2, and NCF4: functional implications.Molecular biology and evolution · 2013Article
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 3 countries.
Funding
Abstract
(•)NO is considered to be a key macrophage-derived cytotoxic effector during Trypanosoma cruzi infection. On the other hand, the microbicidal properties of reactive oxygen species (ROS) are well recognized, but little importance has been attributed to them during in vivo infection with T. cruzi. In order to investigate the role of ROS in T. cruzi infection, mice deficient in NADPH phagocyte oxidase (gp91(phox) (-/-) or phox KO) were infected with Y strain of T. cruzi and the course of infection was followed. phox KO mice had similar parasitemia, similar tissue parasitism and similar levels of IFN-γ and TNF in serum and spleen cell culture supernatants, when compared to wild-type controls. However, all phox KO mice succumbed to infection between day 15 and 21 after inoculation with the parasite, while 60% of wild-type mice were alive 50 days after infection. Further investigation demonstrated increased serum levels of nitrite and nitrate (NOx) at day 15 of infection in phox KO animals, associated with a drop in blood pressure. Treatment with a NOS2 inhibitor corrected the blood pressure, implicating NOS2 in this phenomenon. We postulate that superoxide reacts with (•)NO in vivo, preventing blood pressure drops in wild type mice. Hence, whilst superoxide from phagocytes did not play a critical role in parasite control in the phox KO animals, its production would have an important protective effect against blood pressure decline during infection with T. cruzi.
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