ArticleInternational journal of chronic obstructive pulmonary disease
Cholinergic mechanisms in an organic dust model simulating an acute exacerbation in patients with COPD.
Article in International journal of chronic obstructive pulmonary disease. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 6 citations in OpenAlex.
- De novo discovery of traits co-occurring with chronic obstructive pulmonary disease.Life science alliance · 2023Article
- Evaluation of the microbiome composition in particulate matter inside and outside of pig houses.Journal of animal science and technology · 2021Article
- Change of Serum Inflammatory Cytokines Levels in Patients With Chronic Obstructive Pulmonary Disease, Pneumonia and Lung Cancer.Technology in cancer research & treatmentArticle
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundExposure in a pig barn induces airway inflammation that has similarities with the response observed in acute exacerbations in COPD.
methodsA total of 15 smokers with COPD and 15 healthy non-smokers were exposed for 2 hours in a pig barn (in vivo exposure). Symptoms were assessed, lung function measured, and blood and sputum samples taken before and after exposure. Blood neutrophils were isolated and stimulated ex vivo with dust from a pig barn and acetylcholine, and inflammatory markers were analyzed.
resultsIn vivo exposure caused more symptoms and greater lung function fall in COPD patients than in controls. Baseline concentrations of MMP9, TIMP1, IL6, CXCL8, in sputum and neutrophil blood count were higher in COPD patients than in controls. In vivo exposure increased MMP9, TIMP1, IL6, CXCL8, TNFα, and LTB
conclusionCOPD patients exposed in a pig barn experience symptoms similar to those in acute exacerbations and lung function deterioration that is unrelated to bronchial responsiveness. Cholinergic mechanisms are involved in the inflammatory response to dust, with no difference between COPD and non-smokers.
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