ArticlePloS one2012
Mannose-binding lectin regulates host resistance and pathology during experimental infection with Trypanosoma cruzi.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 17 citations in OpenAlex.
- Quantitative proteomics reveals significant variation in host responses of cattle with differing buffalo fly susceptibility.Frontiers in immunology · 2024Article
- Human Amnion-Derived Mesenchymal Stromal Cells: A New Potential Treatment for Carbapenem-ResistantInternational journal of molecular sciences · 2022Article
- Plasma-Derived Extracellular Vesicles as Potential Biomarkers in Heart Transplant Patient with Chronic Chagas Disease.Emerging infectious diseases · 2020Article
- Article
- Collectins: Innate Immune Pattern Recognition Molecules.Advances in experimental medicine and biology · 2020Review
- Complement Activation by Giardia duodenalis Parasites through the Lectin Pathway Contributes to Mast Cell Responses and Parasite Control.Infection and immunity · 2016Article
- Genetically Determined MBL Deficiency Is Associated with Protection against Chronic Cardiomyopathy in Chagas Disease.PLoS neglected tropical diseases · 2016Article
- Pentraxins and Collectins: Friend or Foe during Pathogen Invasion?Trends in microbiology · 2015Review
- MBL-associated serine proteases (MASPs) and infectious diseases.Molecular immunology · 2015Review
- Deficiency in mannose-binding lectin-associated serine protease-2 does not increase susceptibility to Trypanosoma cruzi infection.The American journal of tropical medicine and hygiene · 2015Article
- Trypanosoma cruzi: Entry into Mammalian Host Cells and Parasitophorous Vacuole Formation.Frontiers in immunology · 2013Article
Corrections and comments
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Authors and funding
9 authors at 6 institutions in 3 countries.
Funding
Abstract
Mannose-binding lectin (MBL) is a humoral pattern-recognition molecule important for host defense. Although recent genetic studies suggest an involvement of MBL/MASP2-associated pathways in Chagas' disease, it is currently unknown whether MBL plays a role in host resistance to the intracellular protozoan Trypanosoma cruzi, the causative agent of Chagas' disease. In this study we employed MBL(-/-) mice to assess the role of MBL in resistance to experimental infection with T. cruzi. T. cruzi infection enhanced tissue expression of MBL both at the mRNA and protein level. Similarly, symptomatic acute Chagas' disease patients displayed increased serum concentrations of MBL compared to patients with indeterminate, asymptomatic forms of the disease. Furthermore, increased parasite loads in the blood and/or tissue were observed in MBL(-/-) mice compared to WT controls. This was associated with reduced systemic levels of IL-12/23p40 in MBL(-/-) mice. Importantly, MBL(-/-) mice infected with a cardiotropic strain of T. cruzi displayed increased myocarditis and cardiac fibrosis compared to WT controls. The latter was accompanied by elevated hydroxyproline content and mRNA levels of collagen-1 and -6 in the heart. These observations point to a previously unappreciated role for MBL in regulating host resistance and cardiac inflammation during infection with a major human pathogen.
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Registered trials
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