Evidence map›Paper›PMID 32667864›Full record

ArticleAmerican journal of physiology. Cell physiology2020

Neutrophil heterogeneity and fate in inflamed tissues: implications for the resolution of inflammation.

János G Filep, Amiram Ariel

Open access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 1 pooled it
4.2field-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

52 citing papers in PubMed, 1 synthesis or guideline pooled it, 76 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Early identification of refractoryFrontiers in medicine · 2026
    Article
  4. Review
  5. Article
  6. Single-Cell Insights Into Macrophage Subtypes in Pulmonary Infections.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
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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

2 authors at 2 institutions in 2 countries.

János G FilepDepartment of Pathology and Cell Biology, University of Montreal and Research Center, Maisonneuve-Rosemont Hospital, Montreal, Quebec, Canada.ORCID 0000-0001-5022-3534
Amiram ArielDepartmentof Biology and Human Biology, University of Haifa, Haifa, Israel.
Hôpital Maisonneuve-Rosemont · CAUniversity of Haifa · IL

Funding

Canadian Institues of Health Research MOP-102619CIHR MOP-97742
6 · The paper itself

Abstract

Neutrophils are polymorphonuclear leukocytes that play a central role in host defense against infection and tissue injury. They are rapidly recruited to the inflamed site and execute a variety of functions to clear invading pathogens and damaged cells. However, many of their defense mechanisms are capable of inflicting collateral tissue damage. Neutrophil-driven inflammation is a unifying mechanism underlying many common diseases. Efficient removal of neutrophils from inflammatory loci is critical for timely resolution of inflammation and return to homeostasis. Accumulating evidence challenges the classical view that neutrophils represent a homogeneous population and that halting neutrophil influx is sufficient to explain their rapid decline within inflamed loci during the resolution of protective inflammation. Hence, understanding the mechanisms that govern neutrophil functions and their removal from the inflammatory locus is critical for minimizing damage to the surrounding tissue and for return to homeostasis. In this review, we briefly address recent advances in characterizing neutrophil phenotypic and functional heterogeneity and the molecular mechanisms that determine the fate of neutrophils within inflammatory loci and the outcome of the inflammatory response. We also discuss how these mechanisms may be harnessed as potential therapeutic targets to facilitate resolution of inflammation.

Indexed as

AnimalsApoptosisHomeostasisHost-Derived Cellular FactorsHumansInflammationNeutrophilsPhenotypeHost-Derived Cellular Factorscell deathefferocytosisneutrophilsneutrophil traffickingspecialized proresolving mediators

Identifiers

PMID32667864
PMCPMC7509268
OpenAlexW3043790623

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.