ArticleBritish journal of pharmacology2008
Therapeutic inhibition of CXCR2 by Reparixin attenuates acute lung injury in mice.
Article in British journal of pharmacology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.
What it found
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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.
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.
Who cites it
82 citing papers in PubMed, 129 citations in OpenAlex.
- A pilot study on reparixin, a CXCR1/2 antagonist, to assess safety and efficacy in attenuating ischaemia-reperfusion injury and inflammation after on-pump coronary artery bypass graft surgery.Clinical and experimental immunology · 2015Trial
- DVT-primed neutrophils reshape the brain microenvironment to promote brain metastasis.bioRxiv : the preprint server for biology · 2026Article
- ERG-deficient endothelium identifies IL-8/CXCR2 axis as a therapeutic target for resolving neutrophilic lung vascular injury.JCI insight · 2026Article
- The Integration of Bioinformatics with Experimental Validation Has Uncovered Shared Molecular Characteristics Between Sarcopenia and Osteoarthritis.Calcified tissue international · 2026Article
- Experimental Models of Acute Lung Injury to Study Inflammation and Pathophysiology: A Narrative Review.Antioxidants (Basel, Switzerland) · 2026Review
- Preliminary results and a theoretical perspective of co‑treatment using a miR‑93‑5p mimic and aged garlic extract to inhibit the expression of the pro‑inflammatory interleukin‑8 gene.Experimental and therapeutic medicine · 2025Article
- Article
- Progesterone amplifies allergic inflammation and airway pathology in association with higher lung ILC2 responses.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- A narrative review of chemokine receptors CXCR1 and CXCR2 and their role in acute respiratory distress syndrome.European respiratory review : an official journal of the European Respiratory Society · 2024Review
- Chemokine expression profile of an innate granuloma.bioRxiv : the preprint server for biology · 2024Article
- Neutrophil Extracellular Traps and Respiratory Disease.Journal of clinical medicine · 2024Review
- Review of COVID-19 Therapeutics by Mechanism: From Discovery to Approval.Journal of Korean medical science · 2024Review
- Peripheral priming induces plastic transcriptomic and proteomic responses in circulating neutrophils required for pathogen containment.Science advances · 2024Article
- Beyond host defense and tissue injury: the emerging role of neutrophils in tissue repair.American journal of physiology. Cell physiology · 2024Review
- Inhaled immunoantimicrobials for the treatment of chronic obstructive pulmonary disease.Science advances · 2024Article
- Genetically Engineered Cellular Nanovesicle as Targeted DNase I Delivery System for the Clearance of Neutrophil Extracellular Traps in Acute Lung Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Efficacy and Safety of Reparixin in Patients with Severe COVID-19 Pneumonia: A Phase 3, Randomized, Double-Blind Placebo-Controlled Study.Infectious diseases and therapy · 2023Article
- Small-molecule chemical probes for the potential therapeutic targets in alcoholic liver diseases.Liver research (Beijing, China) · 2023Review
- Therapeutic inhibition of CXCR1/2: where do we stand?Internal and emergency medicine · 2023Review
- IL-1β Induces a Proinflammatory Fibroblast Microenvironment that Impairs Lung Progenitors' Function.American journal of respiratory cell and molecular biology · 2023Article
22 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 3 countries.
Funding
Abstract
background and purposeAcute lung injury (ALI) remains a major challenge in critical care medicine. Both neutrophils and chemokines have been proposed as key components in the development of ALI. The main chemokine receptor on neutrophils is CXCR2, which regulates neutrophil recruitment and vascular permeability, but no small molecule CXCR2 inhibitor has been demonstrated to be effective in ALI or animal models of ALI. To investigate the functional relevance of the CXCR2 inhibitor Reparixin in vivo, we determined its effects in two models of ALI, induced by either lipopolysaccharide (LPS) inhalation or acid instillation. EXPERIMENTAL APPROACH: In two ALI models in mice, we measured vascular permeability by Evans blue and evaluated neutrophil recruitment into the lung vasculature, interstitium and airspace by flow cytometry. KEY
resultsPharmacological inhibition of CXCR2 by Reparixin reduced CXCL1-induced leukocyte arrest in the microcirculation of the cremaster muscle, but did not influence arrest in response to leukotriene B4 (LTB4) demonstrating specificity. Reparixin (15 microg g(-1)) reduced neutrophil recruitment in the lung by approximately 50% in a model of LPS-induced ALI. A higher dose did not provide additional reduction of neutrophil recruitment. This dose also reduced accumulation of neutrophils in the interstitial compartment and vascular permeability in LPS-induced ALI. Furthermore, both prophylactic and therapeutic application of Reparixin improved gas exchange, and reduced neutrophil recruitment and vascular permeability in a clinically relevant model of acid-induced ALI. CONCLUSIONS AND IMPLICATIONS: Reparixin, a non-competitive allosteric CXCR2 inhibitor attenuates ALI by reducing neutrophil recruitment and vascular permeability.
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Registered trials
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.