Evidence map›Paper›PMID 35112724›Full record

ArticleThe EMBO journal2022

Neutrophils discriminate live from dead bacteria by integrating signals initiated by Fprs and TLRs.

Germana Lentini, Giuseppe Valerio De Gaetano, Agata Famà, Roberta Galbo, Francesco Coppolino, Giuseppe Mancuso, Giuseppe Teti, Concetta Beninati

Open access · greenAbstract read
In one paragraph

Article in The EMBO journal, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

19 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
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  5. Single-cell quantification of the microbiota by flow cytometry: MicFLY.bioRxiv : the preprint server for biology · 2025
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  13. Engagement of αFrontiers in microbiology · 2024
    Article
  14. Oncoimmunology · 2024
    Article
  15. Article
  16. Article
  17. Review
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  19. Anlotinib Benefits theOxidative medicine and cellular longevity · 2022
    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

8 authors at 1 institution in 1 country.

Germana LentiniDepartment of Human Pathology, University of Messina, Messina, Italy.ORCID 0000-0002-0572-4476
Giuseppe Valerio De GaetanoDepartment of Human Pathology, University of Messina, Messina, Italy.
Agata FamàDepartment of Human Pathology, University of Messina, Messina, Italy.
Roberta GalboDepartment of Chemical, Biological and Pharmaceutical Sciences, University of Messina, Messina, Italy.
Francesco CoppolinoDepartment of Biomedical, Dental, Morphological and Functional Imaging Sciences, University of Messina, Messina, Italy.ORCID 0000-0002-9672-0824
Giuseppe MancusoDepartment of Human Pathology, University of Messina, Messina, Italy.
Giuseppe TetiCharybdis Vaccines Srl, Messina, Italy.ORCID 0000-0002-6315-8644
Concetta BeninatiDepartment of Human Pathology, University of Messina, Messina, Italy.
University of Messina · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The mechanisms whereby neutrophils respond differentially to live and dead organisms are unknown. We show here that neutrophils produce 5- to 30-fold higher levels of the Cxcl2 chemokine in response to live bacteria, compared with killed bacteria or isolated bacterial components, despite producing similar levels of Cxcl1 or pro-inflammatory cytokines. Secretion of high levels of Cxcl2, which potently activates neutrophils by an autocrine mechanism, requires three signals. The first two signals are provided by two different sets of signal peptides released by live bacteria, which selectively activate formylated peptide receptor 1 (Fpr1) and Fpr2, respectively. Signal 3 originates from Toll-like receptor activation by microbial components present in both live and killed bacteria. Mechanistically, these signaling pathways converge at the level of the p38 MAP kinase, leading to activation of the AP-1 transcription factor and to Cxcl2 induction. Collectively, our data demonstrate that the simultaneous presence of agonists for Fpr1, Fpr2, and Toll-like receptors represents a unique signature associated with viable bacteria, which is sensed by neutrophils and induces Cxcl2-dependent autocrine cell activation.

Indexed as

AnimalsBacteriaCytokinesFemaleMiceMice, Inbred C57BLMice, KnockoutNeutrophilsProto-Oncogene Proteins c-fesSignal TransductionToll-Like ReceptorsCytokinesProto-Oncogene Proteins c-fesToll-Like Receptorsformylated peptide receptorsinnate immunitylive/dead discriminationneutrophilstoll-like receptors

Identifiers

PMID35112724
PMCPMC8886525
OpenAlexW4210333070

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.