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

journal contribution
posted on 2023-05-18, 03:30 authored by Chen, L, Ge, Q, Tjin, G, Alkhouri, H, Deng, L, Brandsma, C, Adcock, I, Timens, W, Postma, D, Burgess, JK, Black, JL, Oliver, BGG

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-β1. 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.

History

Publication title

The European Respiratory Journal

Volume

44

Pagination

634-646

ISSN

0903-1936

Department/School

Tasmanian School of Medicine

Publisher

European Respiratory Soc Journals Ltd

Place of publication

146 West St, Ste 2.4, Huttons Bldg, Sheffield, England, S1 4Es

Rights statement

Copyright 2014 ERS

Repository Status

  • Restricted

Socio-economic Objectives

Clinical health not elsewhere classified

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