ArticlePLoS neglected tropical diseases2020
NOD2 receptor is crucial for protecting against the digestive form of Chagas disease.
Article in PLoS neglected tropical diseases, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 2 of them syntheses that pooled it.
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Who cites it
5 citing papers in PubMed, 2 syntheses or guidelines pooled it, 6 citations in OpenAlex.
- Distribution, host origin, and transmission cycles of Trypanosoma cruzi genotypes in the State of Rio Grande do Norte, Brazil.Revista da Sociedade Brasileira de Medicina Tropical · 2025Pooled it
- Neuroprotective Treatments for Digestive Forms of Chagas Disease in Experimental Models: A Systematic Review.Oxidative medicine and cellular longevity · 2022Pooled it
- Animal models for exploring Chagas disease pathogenesis and supporting drug discovery.Clinical microbiology reviews · 2024Review
- Molecular and Clinical Aspects of Chronic Manifestations in Chagas Disease: A State-of-the-Art Review.Pathogens (Basel, Switzerland) · 2021Review
- Correlation between intestinal BMP2, IFNγ, and neural death in experimental infection with Trypanosoma cruzi.PloS one · 2021Article
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Authors and funding
13 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Digestive and cardiodigestive forms of Chagas' disease are observed in 2% to 27% of the patients, depending on their geographic location, Trypanosoma cruzi strain and immunopathological responses. The aim of this work was to evaluate the role of NOD2 innate immune receptor in the pathogenesis of the digestive system in Chagas' disease. Patients with digestive form of the disease showed lower mRNA expression of NOD2, higher expression of RIP2 and α-defensin 6, compared to indeterminate form, detected by Real-time PCR in peripheral blood mononuclear cells. In addition, there was a negative correlation between the expression of NOD2 and the degree of dilation of the esophagus, sigmoid and rectum in those patients. The infection of NOD2-/- mice with T. cruzi strain isolated from the digestive patient induced a decrease in intestinal motility. Histopathological analysis of the colon and jejunum of NOD2-/- and wild type C57BL/6 animals revealed discrete inflammatory foci during the acute phase of infection. Interestingly, during the chronic phase of the infection there was inflammation and hypertrophy of the longitudinal and circular muscular layer more pronounced in the colon and jejunum from NOD2-/- animals, when compared to wild type C57BL/6 mice. Together, our results suggest that NOD2 plays a protective role against the development of digestive form of Chagas' disease.
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