ArticleParasite immunology2014
Neutrophils have a protective role during early stages of Leishmania amazonensis infection in BALB/c mice.
Article in Parasite immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 60 citations in OpenAlex.
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- Neutrophil depletion exacerbatesFood and waterborne parasitology · 2026Article
- Neutrophils versus Protozoan Parasites:Microorganisms · 2024Review
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- Paradoxical immune response in leishmaniasis: The role of toll-like receptors in disease progression.Parasite immunology · 2022Review
- Zoonotic Visceral Leishmaniasis: New Insights on Innate Immune Response by Blood Macrophages and Liver Kupffer Cells toBiology · 2022Article
- Interplay of Trypanosome Lytic Factor and innate immune cells in the resolution of cutaneous Leishmania infection.PLoS pathogens · 2021Article
- The Impact of Neutrophil Recruitment to the Skin on the Pathology Induced byFrontiers in immunology · 2021Review
- Resistance AgainstFrontiers in immunology · 2021Article
- The Paradox of a Phagosomal Lifestyle: How Innate Host Cell-Frontiers in immunology · 2021Review
- Visualizing theFrontiers in immunology · 2021Review
- Reconciling protective and pathogenic roles of the NLRP3 inflammasome in leishmaniasis.Immunological reviews · 2020Review
- Obesity impairs resistance to Leishmania major infection in C57BL/6 mice.PLoS neglected tropical diseases · 2020Article
- The state of art of neutrophil extracellular traps in protozoan and helminthic infections.Bioscience reports · 2019Review
- Characterization of immune cell subtypes in three commonly used mouse strains reveals gender and strain-specific variations.Laboratory investigation; a journal of technical methods and pathology · 2019Article
- Cutaneous Leishmaniasis: The Complexity of Host's Effective Immune Response against a Polymorphic Parasitic Disease.Journal of immunology research · 2019Review
- Article
- Resistance ofFrontiers in immunology · 2018Article
- The Src kinases Hck, Fgr and Lyn activate Arg to facilitate IgG-mediated phagocytosis and Leishmania infection.Journal of cell science · 2016Article
- Interleukin-27 (IL-27) Mediates Susceptibility to Visceral Leishmaniasis by Suppressing the IL-17-Neutrophil Response.Infection and immunity · 2016Article
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Neutrophils are involved in the early stages of immune responses to pathogens. Here, we investigated the role of neutrophils during the establishment of Leishmania amazonensis infection in BALB/c and C57BL/6 mice. First, we showed an accumulation of neutrophils between 6 and 24 h post-infection, followed by a reduction in neutrophil numbers after 72 h. Next, we depleted neutrophils prior to infection using RB6-8C5 or 1A8 mAb. Neutrophil depletion led to faster lesion development, increased parasite numbers and higher arginase activity during the first week of infection in BALB/c mice, but not in C57BL/6 mice. Increased susceptibility was accompanied by augmented levels of anti-L. amazonensis IgG and increased production of IL-10 and IL-17. Because IL-10 is a mediator of susceptibility to Leishmania infection, we blocked IL-10 signalling in neutrophil-depleted mice using anti-IL-10R. Interestingly, inhibition of IL-10 signalling abrogated the increase in parasite loads observed in neutrophil-depleted mice, suggesting that parasite proliferation is at least partially mediated by IL-10. Additionally, we tested the effect of IL-17 in inflammatory macrophages and observed that IL-17 increased arginase activity and favoured parasite growth. Taken together, our data indicate that neutrophils control parasite numbers and limit lesion development during the first week of infection in BALB/c mice.
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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.