Author:
Arellano-Orden Elena,Calero-Acuña Carmen,Sanchez-Lopez Verónica,Carrasco-Hernandez Laura,Márquez-Martín Eduardo,Ortega-Ruiz Francisco,Otero-Candelera Remedios,Marín-Hinojosa Carmen,López-Campos José Luis
Abstract
Background: Chronic obstructive pulmonary disease (COPD) is a condition resulting from a persistent inflammatory state in the airways even after smoking cessation. Intriguingly, the reasons behind this persistence of the inflammatory influx without smoking exposure have not been fully unraveled. We aimed to explore the hypothesis that systemic inflammation in COPD patients influences lung cell inflammatory response.
Methods: We cultured human lung fibroblast and human airway epithelial cell lines with plasma from COPD patients (four emphysematous-COPD, four asthma-COPD overlap, four chronic bronchitis-COPD, and four bronchiectasis-COPD), and four smokers or ex-smokers without COPD as controls. We measured Interleukine-8 (IL-8), C-reactive protein (CRP) and matrix metalloproteinase-9 (MMP-9) in plasma and culture supernatants by ELISA.
Results: Cells stimulated with plasma from COPD patients and control subjects produced higher CRP, IL-8 and MMP-9 levels, an increase for COPD in CRP(p=0.039) in epithelial cells and IL-8(p=0.039) in fibroblasts and decrease for MMP-9(p=0.039) in fibroblasts. The response was higher in epithelial cells for IL-8(p=0.003) and in fibroblasts for MMP-9(p=0.063). The plasma from chronic bronchitis and bronchiectasis phenotypes induced higher IL-8 in fibroblasts.
Conclusions: Plasma from COPD patients increases the inflammatory response in lung epithelial cells and lung fibroblasts, with a different response depending on the cell type and clinical phenotype.
Subject
Pulmonary and Respiratory Medicine
Cited by
1 articles.
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