ArticleMediators of inflammation2014
Aspirin modulates innate inflammatory response and inhibits the entry of Trypanosoma cruzi in mouse peritoneal macrophages.
Article in Mediators of inflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.
- Dynamics and functional heterogeneity of FOXP3+ regulatory T cells in Trypanosoma cruzi infection: a systematic review.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Pooled it
- PPAR-γ participates in macrophage polarization induced by Pentatrichomonas hominis.Medical microbiology and immunology · 2026Article
- Towards a map of the immune system manipulation network byFrontiers in cellular and infection microbiology · 2025Review
- Protective role of TRPV1Brain, behavior, & immunity - health · 2024Article
- Immunomodulatory proteins from hookworms reduce cardiac inflammation and modulate regulatory responses in a mouse model of chronicFrontiers in parasitology · 2023Article
- Lipoxin alleviates oxidative stress: a state-of-the-art review.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Review
- The Protective Role of TLR2 Mediates Impaired Autophagic Flux by Activating the mTOR Pathway DuringFrontiers in cellular and infection microbiology · 2021Article
- Combination Therapy Using Benznidazole and Aspirin during the Acute Phase of Experimental Chagas Disease Prevents Cardiovascular Dysfunction and Decreases Typical Cardiac Lesions in the Chronic Phase.Antimicrobial agents and chemotherapy · 2020Article
- ExperimentalFrontiers in immunology · 2020Article
- Cyclooxygenase (COX)-2 Inhibitors ReduceFrontiers in microbiology · 2019Article
- Suppressive Effects of Aspirin for Postthoracotomy Pleural Adhesion in Rats.International journal of medical sciences · 2019Article
- Inflammatory and Pro-resolving Lipids in Trypanosomatid Infections: A Key to Understanding Parasite Control.Frontiers in microbiology · 2018Review
- Extracellular Vesicles Shed ByFrontiers in immunology · 2018Article
- Mass Spectrometry-Based Chemical Cartography of a Cardiac Parasitic Infection.Analytical chemistry · 2017Article
- NLRP3 inflammasome activation in murine macrophages caused by Neospora caninum infection.Parasites & vectors · 2017Article
- Response toFrontiers in microbiology · 2017Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The intracellular protozoan parasite Trypanosoma cruzi causes Chagas disease, a serious disorder that affects millions of people in Latin America. Cell invasion by T. cruzi and its intracellular replication are essential to the parasite's life cycle and for the development of Chagas disease. Here, we present evidence suggesting the involvement of the host's cyclooxygenase (COX) enzyme during T. cruzi invasion. Pharmacological antagonist for COX-1, aspirin (ASA), caused marked inhibition of T. cruzi infection when peritoneal macrophages were pretreated with ASA for 30 min at 37°C before inoculation. This inhibition was associated with increased production of IL-1β and nitric oxide (NO(∙)) by macrophages. The treatment of macrophages with either NOS inhibitors or prostaglandin E2 (PGE2) restored the invasive action of T. cruzi in macrophages previously treated with ASA. Lipoxin ALX-receptor antagonist Boc2 reversed the inhibitory effect of ASA on trypomastigote invasion. Our results indicate that PGE2, NO(∙), and lipoxins are involved in the regulation of anti-T. cruzi activity by macrophages, providing a better understanding of the role of prostaglandins in innate inflammatory response to T. cruzi infection as well as adding a new perspective to specific immune interventions.
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Registered trials
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