ArticlePloS one2010
Inefficient complement system clearance of Trypanosoma cruzi metacyclic trypomastigotes enables resistant strains to invade eukaryotic cells.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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36 citing papers in PubMed, 70 citations in OpenAlex.
- Stage-InformedMicroorganisms · 2026Article
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- Glycocalyx-Driven Immunomodulation in Trypanosoma cruzi: Structures, Host Responses, Diagnostic and Therapeutic Targeting.Parasite immunology · 2026Review
- Chagas disease: host responses, parasite evasion and vaccine advances.Transactions of the Royal Society of Tropical Medicine and Hygiene · 2026Review
- The TcVps34-TcVps15 complex regulates parasite metacyclogenesis and host cell infection inFrontiers in cellular and infection microbiology · 2026Article
- The grand escape - how pathogens outsmart the human complement system.Immunobiology · 2025Review
- Cardiac alterations induced by Trypanosoma cruzi extracellular vesicles and immune complexes.PLoS neglected tropical diseases · 2025Article
- Infectivity of Aflagellar Epimastigotes ofJournal of parasitology research · 2025Article
- Towards a map of the immune system manipulation network byFrontiers in cellular and infection microbiology · 2025Review
- The End Justifies the Means: Chagas Disease from a Perspective of the Host-Life (Basel, Switzerland) · 2024Review
- Mechanisms by which Factor H protectsFrontiers in immunology · 2024Article
- Genome-Wide Libraries for Protozoan Pathogen Drug Target Screening Using Yeast Surface Display.ACS infectious diseases · 2023Article
- Immunopathological Mechanisms Underlying Cardiac Damage in Chagas Disease.Pathogens (Basel, Switzerland) · 2023Review
- Article
- An induced population ofFrontiers in cellular and infection microbiology · 2022Article
- The Liver and the Hepatic Immune Response inPathogens (Basel, Switzerland) · 2021Review
- Comparative Analysis of Virulence Mechanisms of Trypanosomatids Pathogenic to Humans.Frontiers in cellular and infection microbiology · 2021Review
- Is It Possible to Intervene in the Capacity ofFrontiers in immunology · 2021Review
- The Oxidative Stress and Chronic Inflammatory Process in Chagas Disease: Role of Exosomes and Contributing Genetic Factors.Oxidative medicine and cellular longevity · 2021Review
- The role of vascular endothelium and exosomes in human protozoan parasitic diseases.Vessel plus · 2020Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The complement system is the main arm of the vertebrate innate immune system against pathogen infection. For the protozoan Trypanosoma cruzi, the causative agent of Chagas disease, subverting the complement system and invading the host cells is crucial to succeed in infection. However, little attention has focused on whether the complement system can effectively control T. cruzi infection. To address this question, we decided to analyse: 1) which complement pathways are activated by T. cruzi using strains isolated from different hosts, 2) the capacity of these strains to resist the complement-mediated killing at nearly physiological conditions, and 3) whether the complement system could limit or control T. cruzi invasion of eukaryotic cells. The complement activating molecules C1q, C3, mannan-binding lectin and ficolins bound to all strains analysed; however, C3b and C4b deposition assays revealed that T. cruzi activates mainly the lectin and alternative complement pathways in non-immune human serum. Strikingly, we detected that metacyclic trypomastigotes of some T. cruzi strains were highly susceptible to complement-mediated killing in non-immune serum, while other strains were resistant. Furthermore, the rate of parasite invasion in eukaryotic cells was decreased by non-immune serum. Altogether, these results establish that the complement system recognizes T. cruzi metacyclic trypomastigotes, resulting in killing of susceptible strains. The complement system, therefore, acts as a physiological barrier which resistant strains have to evade for successful host infection.
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