Evidence map›Paper›PMID 29345066›Full record

ArticleJournal of leukocyte biology2018

Protease activated-receptor 2 is necessary for neutrophil chemorepulsion induced by trypsin, tryptase, or dipeptidyl peptidase IV.

Michael J V White, Luis E Chinea, Darrell Pilling, Richard H Gomer

Open access · greenAbstract read
In one paragraph

Article in Journal of leukocyte biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.4field-weighted citation impact, top 17% 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

17 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Protease-activated receptor 2 at the intersection of thrombo-inflammation and beyond.International journal of cardiology. Heart & vasculature · 2024
    Article
  5. Article
  6. CD26 and Cancer.Cancers · 2022
    Article
  7. Sex-Based Differences in Human Neutrophil Chemorepulsion.Journal of immunology (Baltimore, Md. : 1950) · 2022
    Article
  8. Article
  9. Article
  10. Article
  11. UsingFrontiers in cell and developmental biology · 2021
    Review
  12. Article
  13. Article
  14. Article
  15. Extracellular signaling in Dictyostelium.The International journal of developmental biology · 2019
    Review
  16. Article
  17. 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

4 authors at 1 institution in 1 country.

Michael J V WhiteDepartment of Biology, Texas A&M University, College Station, Texas, USA.
Luis E ChineaDepartment of Biology, Texas A&M University, College Station, Texas, USA.
Darrell PillingDepartment of Biology, Texas A&M University, College Station, Texas, USA.
Richard H GomerDepartment of Biology, Texas A&M University, College Station, Texas, USA.
Texas A&M University · US

Funding

Pentraxin regulation of macrophage differentiationR01HL118507 · NHLBI · TEXAS A&M UNIVERSITY · PI GOMER, RICHARD H · 2014 to 2017
$1.4M
Elucidation of a eukaryotic chemorepulsion mechanismR01GM118355 · NIGMS · TEXAS A&M UNIVERSITY · PI GOMER, RICHARD H · 2016 to 2019
$1.2M
NHLBI NIH HHS R01 HL118507NIGMS NIH HHS R01 GM118355
6 · The paper itself

Abstract

Compared to neutrophil chemoattractants, relatively little is known about the mechanism neutrophils use to respond to chemorepellents. We previously found that the soluble extracellular protein dipeptidyl peptidase IV (DPPIV) is a neutrophil chemorepellent. In this report, we show that an inhibitor of the protease activated receptor 2 (PAR2) blocks DPPIV-induced human neutrophil chemorepulsion, and that PAR2 agonists such as trypsin, tryptase, 2f-LIGRL, SLIGKV, and AC55541 induce human neutrophil chemorepulsion. Several PAR2 agonists in turn block the ability of the chemoattractant fMLP to attract neutrophils. Compared to neutrophils from male and female C57BL/6 mice, neutrophils from male and female mice lacking PAR2 are insensitive to the chemorepulsive effects of DPPIV or PAR2 agonists. Acute respiratory distress syndrome (ARDS) involves an insult-mediated influx of neutrophils into the lungs. In a mouse model of ARDS, aspiration of PAR2 agonists starting 24 h after an insult reduce neutrophil numbers in the bronchoalveolar lavage (BAL) fluid, as well as the post-BAL lung tissue. Together, these results indicate that the PAR2 receptor mediates DPPIV-induced chemorepulsion, and that PAR2 agonists might be useful to induce neutrophil chemorepulsion.

Indexed as

AnimalsCells, CulturedChemotaxis, LeukocyteDipeptidyl Peptidase 4Disease Models, AnimalFemaleLungMaleMiceMice, Inbred C57BLMice, KnockoutNeutrophilsReceptor, PAR-2Respiratory Distress SyndromeTrypsinTryptasesDipeptidyl Peptidase 4Dpp4 protein, mouseF2rl1 protein, mouseReceptor, PAR-2TrypsinTryptasesacute respiratory distress syndromeARDSchemotaxisDPPIVPAR

Identifiers

PMID29345066
PMCPMC6383205
OpenAlexW2783216831

What OpenQuestion holds

Textmetadata
LicenceTDM
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.