ArticleMicrobes and infection2010
Role of CCL3/MIP-1alpha and CCL5/RANTES during acute Trypanosoma cruzi infection in rats.
Article in Microbes and infection, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.
- Neuroprotective Treatments for Digestive Forms of Chagas Disease in Experimental Models: A Systematic Review.Oxidative medicine and cellular longevity · 2022Pooled it
- Cytokine Profiles and Inflammatory Implications in Chagas Disease: Associations with Ventricular Function and Conduction Disorders.Medical sciences (Basel, Switzerland) · 2025Article
- Chagasic cardiomyopathy is marked by a unique signature of activated CD4Journal of translational medicine · 2022Article
- CCL3/Macrophage Inflammatory Protein-1α Is Dually Involved in Parasite Persistence and Induction of a TNF- and IFNγ-Enriched Inflammatory Milieu inFrontiers in immunology · 2020Article
- Pathogenesis of Chronic Chagas Disease: Macrophages, Mitochondria, and Oxidative Stress.Current clinical microbiology reports · 2018Article
- Potential Role of Carvedilol in the Cardiac Immune Response Induced by Experimental Infection withBioMed research international · 2017Article
- Biomarkers of therapeutic responses in chronic Chagas disease: state of the art and future perspectives.Memorias do Instituto Oswaldo Cruz · 2015Review
- Role of Chemokines and Trafficking of Immune Cells in Parasitic Infections.Current immunology reviews · 2013Article
- Proinflammatory and regulatory cytokines and chemokines in infants with uncomplicated and severe Plasmodium falciparum malaria.Clinical and experimental immunology · 2011Article
- Cavia porcellus as a model for experimental infection by Trypanosoma cruzi.The American journal of pathology · 2011Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
Chagas' disease is caused by Trypanosoma cruzi infection and is characterized by chronic fibrogenic inflammation and heart dysfunction. Chemokines are produced during infection and drive tissue inflammation. In rats, acute infection is characterized by intense myocarditis and regression of inflammation after control of parasitism. We investigated the role of CCL3 and CCL5 during infection by using DNA vaccination encoding for each chemokine separately or simultaneously. MetRANTES treatment was used to evaluate the role of CCR1 and CCR5, the receptors for CCL3 and CCL5. Vaccination with CCL3 or CCL5 increased heart parasitism and decreased local IFN-gamma production, but did not influence intensity of inflammation. Simultaneous treatment with both plasmids or treatment with MetRANTES enhanced cardiac inflammation, fibrosis and parasitism. In conclusion, chemokines CCL3 and CCL5 are relevant, but not essential, for control of T. cruzi infection in rats. On the other hand, combined blockade of these chemokines or their receptors enhanced tissue inflammation and fibrosis, clearly contrasting with available data in murine models of T. cruzi infection. These data reinforce the important role of chemokines during T. cruzi infection but suggest that caution must be taken when expanding the therapeutic modulation of the chemokine system in mice to the human infection.
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