ArticleThe Journal of infectious diseases2014
Understanding the mechanisms controlling Leishmania amazonensis infection in vitro: the role of LTB4 derived from human neutrophils.
Article in The Journal of infectious diseases, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 71 citations in OpenAlex.
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- The impact of probiotic administration in vivo on peritoneal mouse macrophages infected by Leishmania amazonensis ex vivo.Memorias do Instituto Oswaldo Cruz · 2025Article
- Contrasting Phenotypes of Neutrophils During Asymptomatic Versus Symptomatic Leishmania braziliensis Infection.The Journal of infectious diseases · 2024Article
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- Leukotrienes in Innate Immunity: Still Underappreciated after All These Years?Journal of immunology (Baltimore, Md. : 1950) · 2023Review
- Leishmania amazonensis from distinct clinical forms/hosts has polymorphisms in Lipophosphoglycans, displays variations in immunomodulatory properties and, susceptibility to antileishmanial drugs.Cell biology international · 2022Article
- Lipid droplets of protozoan parasites: survival and pathogenicity.Memorias do Instituto Oswaldo Cruz · 2022Article
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- Lipophosphoglycan From Dermotropic New WorldFrontiers in cellular and infection microbiology · 2022Article
- Immune response dynamics and Lutzomyia longipalpis exposure characterize a biosignature of visceral leishmaniasis susceptibility in a canine cohort.PLoS neglected tropical diseases · 2021Article
- Microphysiological Systems for Studying Cellular Crosstalk During the Neutrophil Response to Infection.Frontiers in immunology · 2021Review
- Blockade of TLR2 and TLR4 Attenuates Inflammatory Response and Parasite Load in Cutaneous Leishmaniasis.Frontiers in immunology · 2021Article
- The Paradox of a Phagosomal Lifestyle: How Innate Host Cell-Frontiers in immunology · 2021Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neutrophils are rapidly recruited to the site of Leishmania infection and play an active role in capturing and killing parasites. They are the main source of leukotriene B4 (LTB4), a potent proinflammatory lipid mediator. However, the role of LTB4 in neutrophil infection by Leishmania amazonensis is not clear. In this study, we show that L. amazonensis or its lipophosphoglycan can induce neutrophil activation, degranulation, and LTB4 production. Using pharmacological inhibitors of leukotriene synthesis, our findings reveal an LTB4-driven autocrine/paracrine regulatory effect. In particular, neutrophil-derived LTB4 controls L. amazonensis killing, degranulation, and reactive oxygen species production. In addition, L. amazonensis infection induces an early increase in Toll-like receptor 2 expression, which facilitates parasite internalization. Nuclear factor kappa B (NFkB) pathway activation represents a required upstream event for L. amazonensis-induced LTB4 synthesis. These leishmanicidal mechanisms mediated by neutrophil-derived LTB4 act through activation of its receptor, B leukotriene receptor 1 (BLT1).
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.