ArticleParasites & vectors2019
Role of the lipoxin A4 receptor in the development of neutrophil extracellular traps in Leishmania infantum infection.
Article in Parasites & vectors, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 17 citations in OpenAlex.
- Lipid Mediators in Host-Pathogen Interactions duringACS infectious diseases · 2026Review
- Evaluation of the Cutaneous Immunological Milieu Before and After Treatment With Meglumine Antimoniate in Dogs Naturally Affected by Leishmaniosis due to Leishmania infantum.Veterinary dermatology · 2026Article
- Genomic Regions Associated with Resistance to Gastrointestinal Parasites in Australian Merino Sheep.Genes · 2024Article
- Article
- Determinants of Innate Immunity in Visceral Leishmaniasis and Their Implication in Vaccine Development.Frontiers in immunology · 2021Review
- The State of Art of Extracellular Traps in Protozoan Infections (Review).Frontiers in immunology · 2021Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
backgroundNeutrophils play an immunomodulatory role through the release of neutrophil extracellular traps (NETs). NETs are released in response to Leishmania infection, but the mechanism of NET extrusion has not been elucidated. The lipoxin A4 receptor on neutrophils is crucial for the inflammatory response and immune regulation of many diseases, including Leishmania infection. Therefore, in the present study, we tried to explore whether Leishmania infantum promastigotes stimulate neutrophil activation and NET release via activating the lipoxin A4 receptor.
resultsLeishmania infantum promastigotes stimulated neutrophil activity, but blocking of the lipoxin A4 receptor with its antagonist Boc prior to L. infantum stimulation abrogated these effects. Neutrophils showed citrullinated histone H3 expression and simultaneous NET extrusion on L. infantum stimulation, but a decline in both was observed on blocking of the lipoxin A4 receptor. Moreover, differentiated HL-60 cells with lipoxin A4 receptor silencing showed a decrease in citrullinated histone H3 expression as compared to the unsilenced HL-60 samples on stimulation with promastigotes.
conclusionsLeishmania infantum promastigotes altered the characteristics of neutrophils and induced NET extrusion by activating the lipoxin A4 receptor. The lipoxin A4 receptor may have potential as a therapeutic target in relation to NET extrusion in the treatment of leishmaniasis, but its mechanisms of action need to be explored in more depth.
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