ArticleBritish journal of clinical pharmacology2015
Characterization of the inflammatory response to inhaled lipopolysaccharide in mild to moderate chronic obstructive pulmonary disease.
Article 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 14 papers.
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Who cites it
14 citing papers in PubMed, 26 citations in OpenAlex.
- Dexamethasone inhibits endotoxin-induced coagulopathy in human lungs.Journal of thrombosis and haemostasis : JTH · 2016Trial
- Inflammation induced by inhaled lipopolysaccharide depends on particle size in healthy volunteers.British journal of clinical pharmacology · 2016Trial
- Dissociation between systemic and pulmonary anti-inflammatory effects of dexamethasone in humans.British journal of clinical pharmacology · 2016Trial
- Oral and inhaled p38 MAPK inhibitors: effects on inhaled LPS challenge in healthy subjects.European journal of clinical pharmacology · 2015Trial
- Low-dose multi-walled carbon nanotubes are non-inflammatory alone but amplify lipopolysaccharide-induced cytokine responses in A549 lung epithelial spheroids.Frontiers in immunology · 2026Article
- Computational identification of key genetic drivers in COPD: A first step towards uncovering candidate biomarkers in smokers.Biochemistry and biophysics reports · 2025Article
- Article
- Revisiting Resveratrol as an Osteoprotective Agent: Molecular Evidence from In Vivo and In Vitro Studies.Biomedicines · 2023Review
- The aqueous root extract ofFrontiers in pharmacology · 2023Article
- An inhibitor of RORγ for chronic pulmonary obstructive disease treatment.Scientific reports · 2022Article
- Clinical Experience of Personalized Phage Therapy Against Carbapenem-ResistantFrontiers in cellular and infection microbiology · 2021Article
- Like Cures Like: Pharmacological Activity of Anti-Inflammatory Lipopolysaccharides From Gut Microbiome.Frontiers in pharmacology · 2020Review
- Identification of differentially expressed genes and signaling pathways in chronic obstructive pulmonary disease via bioinformatic analysis.FEBS open bio · 2019Article
- Animal models of emphysema.Chinese medical journal · 2019Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsLipopolysaccharide (LPS) inhalation causes increased airway and systemic inflammation. We investigated LPS inhalation in patients with chronic obstructive pulmonary disease (COPD) as a model of bacterial exacerbations. We studied safety, changes in sputum and systemic biomarkers. We have also investigated interleukin (IL)-17 concentrations in this model.
methodsTwelve COPD patients inhaled 5 μg LPS. Safety was monitored over 24 h. Sputum was induced at baseline, 6 and 24 h for cells and IL-8, IL-17, neutrophil elastase, monocyte chemoattractant protein-1 (MCP-1) and macrophage inflammatory protein-1β (MIP-1β) in supernatants. Serum was collected at baseline, 4, 8 and 24 h for IL-6, C-reactive protein (CRP) and Clara cell protein (CC-16) concentrations. Peripheral blood mononuclear cells (PBMCs) were isolated at baseline and 4 h for systemic IL-17 analysis.
resultsLPS 5 μg was well tolerated. The greatest FEV1 change was 11.7% (mean) at 1 h (95% CI 5.1-18.2%). There was a large range in maximal fall (2.5-37.7%). Total sputum cell count and neutrophil count significantly increased 6 and 24 h post-LPS. There was no change in sputum supernatant mediators. IL-6, CRP and CC-16 increased post-inhalation, with different temporal patterns. CD4+ and CD8+ cell associated IL-17 significantly increased at 4 h.
conclusionsInhaled LPS in COPD patients safely causes increased airway and systemic inflammation. This may be a model for studying COPD exacerbations.
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