Effects of cigarette smoke extract on human airway smooth muscle cells in COPD

Abstract

We hypothesised that the response to cigarette smoke in airway smooth muscle (ASM) cells from smokers with chronic obstructive pulmonary disease (COPD) would be intrinsically different from smokers without COPD, producing greater pro-inflammatory mediators and factors relating to airway remodelling.ASM cells were obtained from smokers with or without COPD, and then stimulated with cigarette smoke extract (CSE) or transforming growth factor-b1. The production of chemokines and matrix metalloproteinases (MMPs) were measured by ELISA, and the deposition of collagens by extracellular matrix ELISA. The effects of CSE on cell attachment and wound healing were measured by toluidine blue attachment and cell tracker green wound healing assays.CSE increased the release of CXCL8 and CXCL1 from human ASM cells, and cells from smokers with COPD produced more CSE-induced CXCL1. The production of MMP-1, -3 and -10, and the deposition of collagen VIII alpha 1 (COL8A1) were increased by CSE, especially in the COPD group which had higher production of MMP-1 and deposition of COL8A1. CSE decreased ASM cell attachment and wound healing in the COPD group only.ASM cells from smokers with COPD were more sensitive to CSE stimulation, which may explain, in part, why some smokers develop COPD. @ERSpublications Cigarette smoke extract induces airway remodelling-associated changes in airway smooth muscle cells in COPD patients

ERS and tobacco harm reduction

“…E-cigarette aerosols can induce acute endothelial cell dysfunction and formation of reactive oxidative stress. Animal studies have shown numerous harmful effects [17][18][19]. Human experiments have shown airway obstruction and dysregulation in normal human lung homeostasis after short-term inhalation [20].…”

Influenza A virus infection and cigarette smoke impair bronchodilator responsiveness to β-adrenoceptor agonists in mouse lung

“…We do not anticipate gross structural changes following in vivo exposure to CS and/or influenza A virus in the present study, as similar models have shown no structural changes to CS and/or influenza A virus model culled at peak viral infection [21,22], and the acute exposure and resolution of inflammation by day 7 post-infection [24]. However, CS or its components have been shown to induce cellular toxicity to a range of cell types including bronchial epithelial cells and airway smooth muscle cells [42–44]. Assessment of reactivity day 7 post-infection (during resolution of inflammation) was chosen to assess whether CS-induced changes following 4 days of exposure [18] would be maintained, and whether changes in reactivity are evident even when viral load has been reduced.…”

Exacerbation of symptomatic arthritis by cigarette smoke in experimental arthritis

“…Cigarette smoke extract (CSE) was prepared as described previously [26]. Briefly, one cigarette (Marlboro red, Phillp Morris, 0.7mg nicotine and 8mg tar) was bubbled through 10ml PBS with a vacuum pump.…”