Evidence map›Paper›PMID 27154356›Full record

ArticleJournal of leukocyte biology2016

Neutrophil extracellular traps release induced by Leishmania: role of PI3Kγ, ERK, PI3Kσ, PKC, and [Ca2+].

Thiago DeSouza-Vieira, Anderson Guimarães-Costa, Natalia C Rochael, Maria N Lira, Michelle T Nascimento, Phillipe de Souza Lima-Gomez, Rafael M Mariante, Pedro M Persechini, Elvira M Saraiva

Open access · bronzeAbstract read
In one paragraph

Article in Journal of leukocyte biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
4.4field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

60 citing papers in PubMed, 94 citations in OpenAlex.

  1. Review
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  4. Article
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  8. Targeting PI3Kγ in cancer.Trends in cancer · 2025
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  9. AMPK and CAMKK activation participate in early events ofFrontiers in veterinary science · 2025
    Article
  10. Article
  11. Review
  12. Exploration (Beijing, China) · 2024
    Review
  13. Article
  14. Article
  15. Review
  16. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

Thiago DeSouza-VieiraLaboratório de Imunobiologia das Leishmanioses, Departamento de Imunologia, Instituto de Microbiologia Paulo de Góes, Universidade Federal do Rio de Janeiro, Brazil.
Anderson Guimarães-CostaLaboratório de Imunobiologia das Leishmanioses, Departamento de Imunologia, Instituto de Microbiologia Paulo de Góes, Universidade Federal do Rio de Janeiro, Brazil.
Natalia C RochaelLaboratório de Imunobiologia das Leishmanioses, Departamento de Imunologia, Instituto de Microbiologia Paulo de Góes, Universidade Federal do Rio de Janeiro, Brazil.
Maria N LiraLaboratório de Imunobiofísica, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Brazil.
Michelle T NascimentoLaboratório de Imunobiologia das Leishmanioses, Departamento de Imunologia, Instituto de Microbiologia Paulo de Góes, Universidade Federal do Rio de Janeiro, Brazil.
Phillipe de Souza Lima-GomezLaboratório de Imunobiologia das Leishmanioses, Departamento de Imunologia, Instituto de Microbiologia Paulo de Góes, Universidade Federal do Rio de Janeiro, Brazil.
Rafael M MarianteLaboratório de Neurogênese, Departamento de Neurobiologia, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Brazil; and Laboratório de Biologia Estrutural, Instituto Oswaldo Cruz, Fiocruz, Brazil.
Pedro M PersechiniLaboratório de Imunobiofísica, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Brazil.
Elvira M SaraivaLaboratório de Imunobiologia das Leishmanioses, Departamento de Imunologia, Instituto de Microbiologia Paulo de Góes, Universidade Federal do Rio de Janeiro, Brazil; esaraiva@micro.ufrj.br.
Universidade Federal do Rio de Janeiro · BRFundação Oswaldo Cruz · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Upon in vitro stimulation, neutrophils undergo a cell death named netosis. This process is characterized by extracellular release of chromatin scaffold associated with granular and cytoplasmic proteins, which together, ensnare and kill microbes. We have previously described that interaction of Leishmania amazonensis with human neutrophils leads to the release of neutrophil extracellular traps, which trap and kill the parasite. However, the signaling leading to Leishmania induced netosis is still unknown. Thus, we sought to evaluate signaling events that drive L. amazonensis induced neutrophil extracellular trap release from human neutrophils. Here, we found that PI3K, independently of protein kinase B, has a role in parasite-induced netosis. We also described that the main isoforms involved are PI3Kγ and PI3Kδ, which work in reactive oxygen species-dependent and -independent ways, respectively. We demonstrated that activation of ERK downstream of PI3Kγ is important to trigger reactive oxygen species-dependent, parasite-induced netosis. Pharmacological inhibition of protein kinase C also significantly decreased parasite-induced neutrophil extracellular trap release. Intracellular calcium, regulated by PI3Kδ, represents an alternative reactive oxygen species-independent pathway of netosis stimulated by L. amazonensis Finally, intracellular calcium mobilization and reactive oxygen species generation are the major regulators of parasite-induced netosis. Our results contribute to a better understanding of the signaling behind netosis induced by interactions between Leishmania and neutrophils.

Indexed as

MAP Kinase Signaling SystemCalcium SignalingChromatinClass Ib Phosphatidylinositol 3-KinaseClass I Phosphatidylinositol 3-KinasesExtracellular TrapsHumansLeishmania mexicanaNeutrophilsPhosphoinositide-3 Kinase InhibitorsPhosphorylationProtein Kinase CProtein Kinase InhibitorsProtein Processing, Post-TranslationalProto-Oncogene Proteins c-aktReactive Oxygen SpeciesChromatinClass Ib Phosphatidylinositol 3-KinaseClass I Phosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsPIK3CD protein, humanPIK3CG protein, humanProtein Kinase CProtein Kinase InhibitorsProto-Oncogene Proteins c-aktReactive Oxygen Speciesnetosisparasitic protozoasignaling

Identifiers

PMID27154356
PMCPMC5014744
OpenAlexW2345346414

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.