ArticleThe American journal of pathology2004
Interferon-gamma-induced nitric oxide causes intrinsic intestinal denervation in Trypanosoma cruzi-infected mice.
Article in The American journal of pathology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.
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Who cites it
42 citing papers in PubMed, 1 synthesis or guideline pooled it, 82 citations in OpenAlex.
- Neuroprotective Treatments for Digestive Forms of Chagas Disease in Experimental Models: A Systematic Review.Oxidative medicine and cellular longevity · 2022Pooled it
- Intermittent suppressive posaconazole therapy is ineffective at mitigating cardiac and digestive tract pathologies in an experimental model of chronic Chagas disease.Antimicrobial agents and chemotherapy · 2025Article
- System-based insights into parasitological and clinical treatment failure in Chagas disease.mSystems · 2025Review
- Animal models for exploring Chagas disease pathogenesis and supporting drug discovery.Clinical microbiology reviews · 2024Review
- Achieving the Optimal AgO Concentrations to Modulate the Anti-Pharmaceutics · 2024Article
- Benznidazole-Loaded Polymeric Nanoparticles for Oral Chemotherapeutic Treatment of Chagas Disease.Pharmaceutics · 2024Article
- Enteric nervous system regeneration and functional cure of experimental digestive Chagas disease with trypanocidal chemotherapy.Nature communications · 2024Article
- The End Justifies the Means: Chagas Disease from a Perspective of the Host-Life (Basel, Switzerland) · 2024Review
- Cardiac Abnormalities in a Predictive Mouse Model of Chagas Disease.Pathogens (Basel, Switzerland) · 2023Article
- Inflammation and mitochondria in the pathogenesis of chronic Chagas disease cardiomyopathy.Experimental biology and medicine (Maywood, N.J.) · 2023Review
- Chagas Disease Megaesophagus Patients Carrying VariantBiomedicines · 2022Article
- A Potential Role of Cholinergic Dysfunction on Impaired Colon Motility in Experimental Intestinal Chagas Disease.Journal of neurogastroenterology and motility · 2022Article
- The Colombian Strain ofMediators of inflammation · 2022Article
- A safe, effective, and reliable vaccine against Chagas disease should be described!Memorias do Instituto Oswaldo Cruz · 2022Article
- Different infective forms trigger distinct lesions in the colon during experimental Chagas disease.Parasitology research · 2021Article
- Local association of Trypanosoma cruzi chronic infection foci and enteric neuropathic lesions at the tissue micro-domain scale.PLoS pathogens · 2021Article
- Host-parasite dynamics in Chagas disease from systemic to hyper-local scales.Parasite immunology · 2021Review
- Correlation between intestinal BMP2, IFNγ, and neural death in experimental infection with Trypanosoma cruzi.PloS one · 2021Article
- The Oxidative Stress and Chronic Inflammatory Process in Chagas Disease: Role of Exosomes and Contributing Genetic Factors.Oxidative medicine and cellular longevity · 2021Review
- Myeloid-Derived Suppressor Cells inFrontiers in cellular and infection microbiology · 2021Review
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In this study, the role of nitric oxide (NO) in neuronal destruction during acute-phase Trypanosoma cruzi infection was evaluated in male C57BL/6 (WT, wild-type) mice and knockout mice [inducible nitric oxide synthase (iNOS)(-/-) and interferon (IFN)(-/-)]. Selected animals were infected by intraperitoneal injection of 100 trypomastigote forms of the Y strain of T. cruzi. Others were injected intraperitoneally with an equal volume of saline solution and served as controls. Our findings support those of previous studies regarding myenteric denervation in acute-phase T. cruzi infection. In addition, we clearly demonstrate that, despite the fact that parasite nests and similar inflammatory infiltrate in the intestinal wall were more pronounced in infected iNOS(-/-) mice than in infected WT mice, the former presented no reduction in myenteric plexus neuron numbers. Neuronal nerve profile expression, as revealed by the general nerve marker PGP 9.5, was preserved in all knockout animals. Infected IFN(-/-) mice suffered no significant neuronal loss and there was no inflammatory infiltrate in the intestinal wall. On days 5 and 10 after infection, iNOS activity was greater in infected WT mice than in controls, whereas iNOS activity in infected knockout mice remained unchanged. These findings clearly demonstrate that neuronal damage does not occur in NO-impaired infected knockout mice, regardless of whether inflammatory infiltrate is present (iNOS(-/-)) or absent (IFN(-/-)). In conclusion, our observations strongly indicate that myenteric denervation in acute-phase T. cruzi infection is because of IFN-gamma-elicited NO production resulting from iNOS activation in the inflammatory foci along the intestinal wall.
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