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

Xiu Mei Wei; Henry S. Kim; Rakesh K. Kumar; Gavin J. Heywood; John E. Hunt; Patrick H. McNeil; Paul S. Thomas

doi:10.1186/1465-9921-6-108

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

Xiu Mei Wei, Henry S. Kim, Rakesh K. Kumar, Gavin J. Heywood, John E. Hunt, Patrick H. McNeil, Paul S. Thomas^*

^*Corresponding author for this work

Research output: Contribution to journal › Article › peer-review

30 Citations (Scopus)

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.

Original language	English
Article number	108
Pages (from-to)	1-9
Number of pages	9
Journal	Respiratory Research
Volume	6
DOIs	https://doi.org/10.1186/1465-9921-6-108
Publication status	Published - 19 Sept 2005
Externally published	Yes

Keywords

Cigarette smoke
Epithelial cells
Mast cells
Nitric oxide

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10.1186/1465-9921-6-108

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title = "Effects of cigarette smoke on degranulation and NO production by mast cells and epithelial cells",

abstract = "Exhaled nitric oxide (eNO) is decreased by cigarette smoking. The hypothesis that oxides of nitrogen (NOx ) 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 NOx -related negative feedback.",

keywords = "Cigarette smoke, Epithelial cells, Mast cells, Nitric oxide",

author = "Wei, {Xiu Mei} and Kim, {Henry S.} and Kumar, {Rakesh K.} and Heywood, {Gavin J.} and Hunt, {John E.} and McNeil, {Patrick H.} and Thomas, {Paul S.}",

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doi = "10.1186/1465-9921-6-108",

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AU - Wei, Xiu Mei

AU - Kim, Henry S.

AU - Kumar, Rakesh K.

AU - Heywood, Gavin J.

AU - Hunt, John E.

AU - McNeil, Patrick H.

AU - Thomas, Paul S.

PY - 2005/9/19

Y1 - 2005/9/19

N2 - Exhaled nitric oxide (eNO) is decreased by cigarette smoking. The hypothesis that oxides of nitrogen (NOx ) 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 NOx -related negative feedback.

AB - Exhaled nitric oxide (eNO) is decreased by cigarette smoking. The hypothesis that oxides of nitrogen (NOx ) 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 NOx -related negative feedback.

KW - Cigarette smoke

KW - Epithelial cells

KW - Mast cells

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

Abstract

Keywords

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