Trial reportBritish journal of clinical pharmacology2015
The effect of a selective CXCR2 antagonist (AZD5069) on human blood neutrophil count and innate immune functions.
Trial report in British journal of clinical pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 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
48 citing papers in PubMed.
- A window-of-opportunity trial of the CXCR1/2 inhibitor reparixin in operable HER-2-negative breast cancer.Breast cancer research : BCR · 2020Trial
- Pharmacokinetics of the Oral Selective CXCR2 Antagonist AZD5069: A Summary of Eight Phase I Studies in Healthy Volunteers.Drugs in R&D · 2018Trial
- Trial
- The effect of a selective CXCR2 antagonist (AZD5069) on human blood neutrophil count and innate immune functions.British journal of clinical pharmacology · 2015Trial
- Article
- Different Inflammatory Phenotypes and Immune Endotypes Drive Disease Heterogeneity in Asthma and COPD.Clinical reviews in allergy & immunology · 2026Review
- From steatosis to metastasis: microenvironmental reprogramming of the liver in metabolic dysfunction-associated steatotic liver disease.Clinical and molecular hepatology · 2026Review
- Harnessing myeloid cell plasticity for cancer therapy.Nature cancer · 2026Review
- Trajectory-Based Clustering to Identify Asthma Subgroups Responsive to the Selective CXCR2 Antagonist, AZD5069.Allergy · 2026Article
- Neutrophil Heterogeneity in Airway Inflammatory Diseases.Inflammation · 2025Review
- Allergic Contact Dermatitis: Immunopathology and Potential Therapeutic Strategies.Journal of clinical medicine · 2025Review
- Targeting CXCR2 signaling in inflammatory lung diseases: neutrophil-driven inflammation and emerging therapies.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Selective anti-CXCR2 receptor blockade by AZD5069 inhibits CXCL8-mediated pro-tumorigenic activity in human thyroid cancer cells in vitro.Journal of endocrinological investigation · 2025Article
- CXCR4 antagonism corrects neutrophil abnormalities and reduces pneumonia severity in a pharmacological mouse model of CXCR2 loss-of-function-mediated neutropenia.Frontiers in immunology · 2025Article
- A key regulator of tumor-associated neutrophils: the CXCR2 chemokine receptor.Journal of molecular histology · 2024Review
- Targeting immune cell recruitment in atherosclerosis.Nature reviews. Cardiology · 2024Review
- Targeting IL-8 and Its Receptors in Prostate Cancer: Inflammation, Stress Response, and Treatment Resistance.Cancers · 2024Review
- A microphysiological system reveals neutrophil contact-dependent attenuation of pancreatic tumor progression by CXCR2 inhibition-based immunotherapy.Scientific reports · 2024Article
- Molecular insights of exercise therapy in disease prevention and treatment.Signal transduction and targeted therapy · 2024Review
- Neutrophils in Physiology and Pathology.Annual review of pathology · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
aimsThe aim of the present study was to investigate whether selective antagonism of the cysteine-X-cysteine chemokine receptor-2 (CXCR2) receptor has any adverse effects on the key innate effector functions of human neutrophils for defence against microbial pathogens.
methodsIn a double-blind, crossover study, 30 healthy volunteers were randomized to treatment with the CXCR2 antagonist AZD5069 (100 mg) or placebo, twice daily orally for 6 days. The peripheral blood neutrophil count was assessed at baseline, daily during treatment and in response to exercise challenge and subcutaneous injection of granulocyte-colony stimulating factor (G-CSF). Neutrophil function was evaluated by phagocytosis of Escherichia coli and by the oxidative burst response to E. coli.
resultsAZD5069 treatment reversibly reduced circulating neutrophil count from baseline by a mean [standard deviation (SD)] of -1.67 (0.67) ×10(9) l(-1) vs. 0.19 (0.78) ×10(9) l(-1) for placebo on day 2, returning to baseline by day 7 after the last dose. Despite low counts on day 4, a 10-min exercise challenge increased absolute blood neutrophil count, but the effect with AZD5069 was smaller and not sustained, compared with placebo treatment. Subcutaneous G-CSF on day 5 caused a substantial increase in blood neutrophil count in both placebo- and AZD5069-treated subjects. Superoxide anion production in E. coli-stimulated neutrophils and phagocytosis of E. coli were unaffected by AZD5069 (P = 0.375, P = 0.721, respectively vs. baseline, Day 4). AZD5069 was well tolerated.
conclusionsCXCR2 antagonism did not appear adversely to affect the mobilization of neutrophils from bone marrow into the peripheral circulation, phagocytosis or the oxidative burst response to bacterial pathogens. This supports the potential of CXCR2 antagonists as a treatment option for diseases in which neutrophils play a pathological role.
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