Evidence map›Paper›PMID 35274151›Full record

ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2022

Protease-activated receptor 2 enhances innate and inflammatory mechanisms induced by lipopolysaccharide in macrophages from C57BL/6 mice.

Ayslan Barra, Amanda Ferreira Brasil, Thaís Lemos Ferreira, Weslley Fernandes-Braga, Danielle Gomes Marconato, Priscila Faria-Pinto, Jacqueline Isaura Alvarez-Leite, Luciano Dos Santos Aggum Capettini, André Klein

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In one paragraph

Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Current perspectives on the pathogenesis of cerebral atherosclerosis.Journal of inflammation (London, England) · 2025
    Review
  2. Article
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.

Ayslan BarraLaboratory of Pain and Inflammation, Department of Pharmacology, Institute of Biological Sciences (ICB), Federal University of Minas Gerais (UFMG), Av. Presidente Antônio Carlos, 6627, Pampulha, Belo Horizonte, Minas Gerais, 31270-901, Brazil.
Amanda Ferreira BrasilLaboratory of Pain and Inflammation, Department of Pharmacology, Institute of Biological Sciences (ICB), Federal University of Minas Gerais (UFMG), Av. Presidente Antônio Carlos, 6627, Pampulha, Belo Horizonte, Minas Gerais, 31270-901, Brazil.
Thaís Lemos FerreiraLaboratory of Vascular Biology, ICB/UFMG, Belo Horizonte, Minas Gerais, Brazil.
Weslley Fernandes-BragaLaboratory of Atherosclerosis and Nutritional Biochemistry (LABIN-UFMG), Department of Biochemistry and Immunology, ICB/UFMG, Belo Horizonte, Minas Gerais, Brazil.
Danielle Gomes MarconatoDepartment of Biochemistry, Federal University of Juiz de Fora (UFJF), Juiz de Fora, Minas Gerais, Brazil.
Priscila Faria-PintoDepartment of Biochemistry, Federal University of Juiz de Fora (UFJF), Juiz de Fora, Minas Gerais, Brazil.
Jacqueline Isaura Alvarez-LeiteLaboratory of Atherosclerosis and Nutritional Biochemistry (LABIN-UFMG), Department of Biochemistry and Immunology, ICB/UFMG, Belo Horizonte, Minas Gerais, Brazil.
Luciano Dos Santos Aggum CapettiniLaboratory of Vascular Biology, ICB/UFMG, Belo Horizonte, Minas Gerais, Brazil.
André KleinLaboratory of Pain and Inflammation, Department of Pharmacology, Institute of Biological Sciences (ICB), Federal University of Minas Gerais (UFMG), Av. Presidente Antônio Carlos, 6627, Pampulha, Belo Horizonte, Minas Gerais, 31270-901, Brazil. klein@ufmg.br.ORCID http://orcid.org/0000-0001-9788-4647

Funding

Fundação de Amparo à Pesquisa do Estado de Minas Gerais PPM-00593-16
6 · The paper itself

Abstract

objectiveThis study was conducted to investigate the effects of the synthetic PAR2 agonist peptide (PAR2-AP) SLIGRL-NH

methodsPeritoneal macrophages obtained from C57BL/6 mice were incubated with PAR2-AP and/or LPS, and the phagocytosis of zymosan fluorescein isothiocyanate (FITC) particles; nitric oxide (NO), reactive oxygen species (ROS), and cytokine production; and inducible NO synthase (iNOS) expression in macrophages co-cultured with PAR-2-AP/LPS were evaluated.

resultsCo-incubation of macrophages with PAR2AP (30 µM)/LPS (100 ng/mL) enhanced LPS-induced phagocytosis; production of NO, ROS, and the pro-inflammatory cytokines interleukin (IL)-1β, tumour necrosis factor (TNF)-α, IL-6, and C-C motif chemokine ligand (CCL)2; and iNOS expression and impaired the release of the anti-inflammatory cytokine IL-10 after 4 h of co-stimulation. In addition, PAR2AP increased the LPS-induced translocation of the p65 subunit of the pro-inflammatory transcription factor nuclear factor kappa B (NF-κB) and reduced the expression of inhibitor of NF-κB.

conclusionThis study provides evidence of a role for PAR2 in macrophage response triggered by LPS enhancing the phagocytic activity and NO, ROS, and cytokine production, resulting in the initial and adequate macrophage response required for their innate response mechanisms.

Indexed as

LipopolysaccharidesNF-kappa BAnimalsCytokinesMacrophagesMiceMice, Inbred C57BLNitric OxideNitric Oxide Synthase Type IIReactive Oxygen SpeciesReceptor, PAR-2Tumor Necrosis Factor-alphaCytokinesF2rl1 protein, mouseLipopolysaccharidesNF-kappa BNitric OxideNitric Oxide Synthase Type IIReactive Oxygen SpeciesReceptor, PAR-2Tumor Necrosis Factor-alphaLPSMacrophagesPAR2

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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.