%0 Journal Article
%T Cigarette smoke induces IL-8, but inhibits eotaxin and RANTES release from airway smooth muscle
%A Ute Oltmanns
%A Kian F Chung
%A Matthew Walters
%A Matthias John
%A Jane A Mitchell
%J Respiratory Research
%D 2005
%I BioMed Central
%R 10.1186/1465-9921-6-74
%X HASMC in primary culture were exposed to cigarette smoke extract (CSE) with or without TNF¦Á. Chemokines were measured by enzyme-linked immunosorbent assay (ELISA) and gene expression by real time polymerase chain reaction (PCR). Data were analysed using one-way analysis of variance (ANOVA) followed by Bonferroni's t testCSE (5, 10 and 15%) induced IL-8 release and expression without effect on eotaxin or RANTES release. At 20%, there was less IL-8 release. TNF¦Á enhanced CSE-induced IL-8 release and expression. However, CSE (5¨C30%) inhibited TNF¦Á-induced eotaxin and RANTES production. The effects of CSE on IL-8 release were inhibited by glutathione (GSH) and associated with the induction of the oxidant sensing protein, heme oxygenase-1.Cigarette smoke may directly cause the release of IL-8 from HASMC, an effect enhanced by TNF-¦Á which is overexpressed in COPD. Inhibition of eotaxin and RANTES by cigarette smoke is consistent with the predominant neutrophilic but not eosinophilic inflammation found in COPD.Chronic obstructive pulmonary disease (COPD) is a major public health problem that is currently ranking as the fourth leading cause of death in the world [1]. It is characterised by progressive and largely irreversible airflow limitation associated with symptoms such as cough, sputum production, and dyspnea. A chronic inflammatory response of the lung to noxious particles, most notably tobacco smoke, but also occupational dusts and air pollution, is currently considered as the underlying pathological mechanism leading to this clinical condition [1]. However, the link between inhalation of harmful substances, such as cigarette smoke, bronchial inflammation and the development of airflow limitation is not completely understood.Currently, cessation of smoking is the only intervention that slows down disease progression in COPD [2]. Although only a minority of smokers develop symptoms of COPD, there is evidence that even in the lungs of asymptomatic smokers the numbers o
%U http://respiratory-research.com/content/6/1/74