Evidence map›Paper›PMID 39048127›Full record

ReviewEuropean respiratory review : an official journal of the European Respiratory Society2024

A narrative review of chemokine receptors CXCR1 and CXCR2 and their role in acute respiratory distress syndrome.

Sophie Toya, Sofie Struyf, Luis Huerta, Peter Morris, Elizabeth Gavioli, Enrico Maria Minnella, Maria Candida Cesta, Marcello Allegretti, Paul Proost

Abstract readReview
In one paragraph

Review in European respiratory review : an official journal of the European Respiratory Society, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing 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

20 citing papers in PubMed.

  1. A novel CXCL8(3-72) K11R/G31P-BPIEmerging microbes & infections · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Host-pathogen-immune interactions in an air-liquid interface airway model.Frontiers in cellular and infection microbiology · 2026
    Article
  13. Article
  14. Review
  15. Article
  16. CXCR1 Depletion in Ly6CAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  17. Article
  18. Article
  19. Review
  20. 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.

Sophie ToyaDompé Farmaceutici S.p.A, Milan, Italy sophie.toya@dompe.com.
Sofie StruyfKU Leuven, Department of Microbiology, Immunology and Transplantation, Leuven, Belgium.
Luis HuertaKeck School of Medicine of USC, Department of Medicine, Pulmonary and Critical Care Medicine, Los Angeles, CA, USA.
Peter MorrisThe University of Alabama at Birmingham, Department of Medicine, Pulmonary, Allergy, and Critical Care Medicine, Birmingham, AL, USA.
Elizabeth GavioliDompé Farmaceutici S.p.A, Milan, Italy.
Enrico Maria MinnellaDompé Farmaceutici S.p.A, Milan, Italy.
Maria Candida CestaDompé Farmaceutici S.p.A, Milan, Italy.
Marcello AllegrettiDompé Farmaceutici S.p.A, Milan, Italy.
Paul ProostKU Leuven, Department of Microbiology, Immunology and Transplantation, Leuven, Belgium.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute respiratory distress syndrome (ARDS) is a severe form of acute respiratory failure characterised by extensive inflammatory injury to the alveolocapillary barrier leading to alveolar oedema, impaired gas exchange and, ultimately, hypoxaemia necessitating the use of supplemental oxygen combined with some degree of positive airway pressure. Although much heterogeneity exists regarding the aetiology, localisation and endotypic characterisation of ARDS, what remains largely undisputed is the role of the innate immune system, and in particular of neutrophils, in precipitating and propagating lung injury. Activated neutrophils, recruited to the lung through chemokine gradients, promote injury by releasing oxidants, proteases and neutrophil extracellular traps, which ultimately cause platelet aggregation, microvascular thrombosis and cellular death. Among various neutrophilic chemoattractants, interleukin-8/C-X-C motif ligand 8 and related chemokines, collectively called ELR+ chemokines, acting on neutrophils through the G protein-coupled receptors CXCR1 and CXCR2, are pivotal in orchestrating the neutrophil activation status and chemotaxis in the inflamed lung. This allows efficient elimination of infectious agents while at the same time minimising collateral damage to host tissue. Therefore, understanding how CXCR1 and CXCR2 receptors are regulated is important if we hope to effectively target them for therapeutic use in ARDS. In the following narrative review, we provide an overview of the role of ELR+ chemokines in acute lung injury (ALI) and ARDS, we summarise the relevant regulatory pathways of their cognisant receptors CXCR1/2 and highlight current preclinical and clinical evidence on the therapeutic role of CXCR1 and CXCR2 inhibition in animal models of ALI, as well as in ARDS patients.

Indexed as

LungNeutrophilsReceptors, Interleukin-8AReceptors, Interleukin-8BRespiratory Distress SyndromeSignal TransductionAnimalsHumansNeutrophil ActivationNeutrophil InfiltrationCXCR2 protein, humanReceptors, Interleukin-8AReceptors, Interleukin-8B

Identifiers

PMID39048127
PMCPMC11267298

What OpenQuestion holds

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LicenceCC BY-NC
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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.