ArticlePulmonary pharmacology & therapeutics2015
CXCR1/CXCR2 antagonist CXCL8(3-74)K11R/G31P blocks lung inflammation in swine barn dust-instilled mice.
Article in Pulmonary pharmacology & therapeutics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 13 citations in OpenAlex.
- The diagnostic value of CXCL8 in diabetes mellitus co-morbidity with tuberculosis.BMC infectious diseases · 2026Article
- CXCR1 Depletion in Ly6CAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Alveolar epithelial and vascular CXCR2 mediates transcytosis of CXCL1 in inflamed lungs.Nature communications · 2025Article
- 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
- Therapeutic inhibition of CXCR1/2: where do we stand?Internal and emergency medicine · 2023Review
- Porcine CXCR1/2 antagonist CXCL8Scientific reports · 2020Article
- Effects of glycyrrhizin on lipopolysaccharide-induced acute lung injury in a mouse model.Journal of thoracic disease · 2019Article
- Ethyl pyruvate reduces organic dust-induced airway inflammation by targeting HMGB1-RAGE signaling.Respiratory research · 2019Article
- Kinome analyses of inflammatory responses to swine barn dust extract in human bronchial epithelial and monocyte cell lines.Innate immunity · 2018Article
- Article
- Genetic Ablation of CXCR2 Protects against Cigarette Smoke-Induced Lung Inflammation and Injury.Frontiers in pharmacology · 2016Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Inhalation of agricultural occupational dusts from swine confinement facilities can result in lung inflammation. The innate immune response to organic barn dusts results in production of a number of pro-inflammatory factors in the lungs of barn workers such as cytokines, chemokines, and an influx of neutrophils. Many of these inflammatory factors are influenced by the chemokine CXCL8/IL-8 (KC or MIP-2 in mice). Previously, we have demonstrated that an endotoxin-independent component of swine barn dust extract (SBE) elevates lung chemokines in a protein kinase C (PKC)-dependent manner resulting in the significant formation of lung inflammatory cell infiltrates in a mouse model of SBE injury. In this study we test the ability of a CXCR1/CXCR2 antagonist, CXCL8(3-74)K11R/G31P (G31P) to block many of the features of lung-inflammation in response to challenge with SBE in an established mouse exposure system. Injection of G31P concurrent with SBE nasal instillation over a course of 3 weeks significantly reduced neutrophil accumulation in the lungs of barn dust exposed animals compared to those given SBE alone. There was a similar reduction in pro-inflammatory cytokines and chemokines IL-6, KC, and MIP-2 in SBE plus G31P-treated mice. In addition to excreted products, the receptors ICAM-1, CXCR1, and CXCR2, which all were elevated with SBE exposure, were also decreased with G31P treatment. SBE activation of PKCα and PKCε was reduced as well with G31P treatment. Thus, G31P was found to be highly effective at reducing several features of lung inflammation in mice exposed to barn dust extracts.
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Registered trials
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