Research

Effects of cigarette smoke on degranulation and NO production by mast cells and epithelial cells

Xiu M Wei¹ , Henry S Kim¹ , Rakesh K Kumar¹ , Gavin J Heywood¹ , John E Hunt¹ , H Patrick McNeil¹ and Paul S Thomas^1,2

¹  Inflammation Research Unit, School of Pathology, Faculty of Medicine, UNSW, Sydney, Australia

²  Department of Respiratory Medicine, Prince of Wales Hospital, Randwick, NSW, 2031, Australia

author email corresponding author email

Respiratory Research 2005, 6:108doi:10.1186/1465-9921-6-108

Published:	19 September 2005

Abstract

Exhaled nitric oxide (eNO) is decreased by cigarette smoking. The hypothesis that oxides of nitrogen (NO_X) in cigarette smoke solution (CSS) may exert a negative feedback mechanism upon NO release from epithelial (AEC, A549, and NHTBE) and basophilic cells (RBL-2H3) was tested in vitro. CSS inhibited both NO production and degranulation (measured as release of beta-hexosaminidase) in a dose-dependent manner from RBL-2H3 cells. Inhibition of NO production by CSS in AEC, A549, and NHTBE cells was also dose-dependent. In addition, CSS decreased expression of NOS mRNA and protein expression. The addition of NO inhibitors and scavengers did not, however, reverse the effects of CSS, nor did a NO donor (SNP) or nicotine mimic CSS. N-acetyl-cysteine, partially reversed the inhibition of beta-hexosaminidase release suggesting CSS may act via oxidative free radicals. Thus, some of the inhibitory effects of CSS appear to be via oxidative free radicals rather than a NO_X -related negative feedback.