ArticleAmerican journal of physiology. Lung cellular and molecular physiology2005
Role of CXCR2 in cigarette smoke-induced lung inflammation.
Article in American journal of physiology. Lung cellular and molecular physiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.
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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.
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Who cites it
69 citing papers in PubMed, 163 citations in OpenAlex.
- The effect of a selective CXCR2 antagonist (AZD5069) on human blood neutrophil count and innate immune functions.British journal of clinical pharmacology · 2015Trial
- An aberrant leukotriene A4 hydrolase-proline-glycine-proline pathway in the pathogenesis of chronic obstructive pulmonary disease.American journal of respiratory and critical care medicine · 2014Trial
- Biomarkers in COPD-Associated PH/CCP: Circulating Molecules and Cell-Intrinsic Marker.International journal of chronic obstructive pulmonary disease · 2025Review
- Exposure to air pollution increases susceptibility to ulcerative colitis through epigenetic alterations in CXCR2 and MHC class III region.EBioMedicine · 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
- Identification of novel biomarkers related to neutrophilic inflammation in COPD.Frontiers in immunology · 2024Article
- Therapeutic inhibition of CXCR1/2: where do we stand?Internal and emergency medicine · 2023Review
- The chemokines CXCL8 and CXCL12: molecular and functional properties, role in disease and efforts towards pharmacological intervention.Cellular & molecular immunology · 2023Review
- NLRP6 controls pulmonary inflammation from cigarette smoke in a gut microbiota-dependent manner.Frontiers in immunology · 2023Article
- Novel Anti-Inflammatory Approaches to COPD.International journal of chronic obstructive pulmonary disease · 2023Review
- Dung biomass smoke exposure impairs resolution of inflammatory responses to influenza infection.Toxicology and applied pharmacology · 2022Article
- In Vivo and In Vitro Studies of Cigarette Smoke Effects on Innate Responses to Influenza Virus: A Matter of Models?Viruses · 2022Review
- Targeting the alternative oxidase (AOX) for human health and food security, a pharmaceutical and agrochemical target or a rescue mechanism?The Biochemical journal · 2022Review
- A 6-month inhalation toxicology study in ApoeArchives of toxicology · 2021Article
- Neutrophil-Dependent Immunity During Pulmonary Infections and Inflammations.Frontiers in immunology · 2021Review
- Relationship Between Proteinase with a Disintegrin and a Metalloproteinase Domain-9 (ADAM9), Inflammation, Airway Remodeling, and Emphysema in COPD Patients.International journal of chronic obstructive pulmonary disease · 2020Article
- Machine Learning Approach for Predicting Past Environmental Exposures From Molecular Profiling of Post-Exposure Human Serum Samples.Journal of occupational and environmental medicine · 2019Article
- IL-22 and its receptors are increased in human and experimental COPD and contribute to pathogenesis.The European respiratory journal · 2019Article
- Chemokines in COPD: From Implication to Therapeutic Use.International journal of molecular sciences · 2019Review
- Alternative Oxidase Attenuates Cigarette Smoke-induced Lung Dysfunction and Tissue Damage.American journal of respiratory cell and molecular biology · 2019Article
9 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
10 authors at 1 institution in 1 country.
Funding
Abstract
It has been hypothesized that the destruction of lung tissue observed in smokers with chronic obstructive pulmonary disease and emphysema is mediated by neutrophils recruited to the lungs by smoke exposure. This study investigated the role of the chemokine receptor CXCR2 in mediating neutrophilic inflammation in the lungs of mice acutely exposed to cigarette smoke. Exposure to dilute mainstream cigarette smoke for 1 h, twice per day for 3 days, induced acute inflammation in the lungs of C57BL/6 mice, with increased neutrophils and the neutrophil chemotactic CXC chemokines macrophage inflammatory protein (MIP)-2 and KC. Treatment with SCH-N, an orally active small molecule inhibitor of CXCR2, reduced the influx of neutrophils into the bronchoalveolar lavage (BAL) fluid. Histological changes were seen, with drug treatment reducing perivascular inflammation and the number of tissue neutrophils. beta-Glucuronidase activity was reduced in the BAL fluid of mice treated with SCH-N, indicating that the reduction in neutrophils was associated with a reduction in tissue damaging enzymes. Interestingly, whereas MIP-2 and KC were significantly elevated in the BAL fluid of smoke exposed mice, they were further elevated in mice exposed to smoke and treated with drug. The increase in MIP-2 and KC with drug treatment may be due to the decrease in lung neutrophils that either are not present to bind these chemokines or fail to provide a feedback signal to other cells producing these chemokines. Overall, these results demonstrate that inhibiting CXCR2 reduces neutrophilic inflammation and associated lung tissue damage due to acute cigarette smoke exposure.
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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.