2001
DOI: 10.1096/fsb2fj000432fje
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Cigarette smoking reduces histone deacetylase 2 expression, enhances cytokine expression, and inhibits glucocorticoid actions in alveolar macrophages

Abstract: Cigarette smoke is the major cause of chronic obstructive pulmonary disease (COPD), a chronic inflammatory disease of the airway. The increased expression of inflammatory proteins results from enhanced gene transcription, as these mediators are induced in a cell‐specific manner. Changes in transcription depend on chromatin remodeling and the relative activities of histone acetyl‐transferases (HATs) and histone deacetylases (HDACs). We have shown that cigarette smoke reduces the expression of HDAC2 expression a… Show more

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Cited by 168 publications
(93 citation statements)
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References 38 publications
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“…The inhibition of the IL-8 release by DEX in the H 2 O 2 -pretreated and poly(I:C)-exposed cells was less than in the vehicle-pretreated and poly(I:C)-exposed cells, suggesting that oxidative stress reduces the effect of steroid on the IL-8 release. The acquirement of steroid resistance under oxidative stress has been reported to occur in macrophages and epithelial cells via inactivation of histone deacetylase 2 (HDAC2) (34,45). This inactivation of HDAC2 by oxidative stress might explain our result that DEX was less effective in the H 2 O 2 -treated cells.…”
Section: Discussionmentioning
confidence: 57%
See 1 more Smart Citation
“…The inhibition of the IL-8 release by DEX in the H 2 O 2 -pretreated and poly(I:C)-exposed cells was less than in the vehicle-pretreated and poly(I:C)-exposed cells, suggesting that oxidative stress reduces the effect of steroid on the IL-8 release. The acquirement of steroid resistance under oxidative stress has been reported to occur in macrophages and epithelial cells via inactivation of histone deacetylase 2 (HDAC2) (34,45). This inactivation of HDAC2 by oxidative stress might explain our result that DEX was less effective in the H 2 O 2 -treated cells.…”
Section: Discussionmentioning
confidence: 57%
“…Four strains of primary human bronchial epithelial cells (HBEpC) were purchased from Cell Aplications, Inc. (San Diego, CA) and ScienCell research laboratories (Carlsbad, CA). BEAS-2B cells (passages [45][46][47][48][49][50][51][52][53][54][55] or HBEpC (passages 3-7) were cultured in serum-free Keratinocyte Basal Medium supplemented with 10 ng/ml recombinant epidermal growth factor and 30 mg/ml bovine pituitary extract. Cells were cultured at 378C in a humidified atmosphere of 5% CO 2 and passaged.…”
Section: Preparation Of Epithelial Cellsmentioning
confidence: 99%
“…In asthmatic airways, there is an increase in NF-kB activation and an increase in HAT activity [26,27]. Histone acetylation is reversed by HDACs, and there is a reduction in HDAC activity in asthmatic airways and in COPD [27][28][29]. Many of the most frequent lung diseases, including cystic fibrosis, interstitial lung disease and acute respiratory distress syndrome, involve inflammation with the co-ordinate expression of multiple inflammatory genes in the lungs.…”
Section: Discussionmentioning
confidence: 99%
“…There are a number of other potential mechanisms by which cigarette smoking may induce insensitivity to corticosteroids. Experimental findings suggest down-regulation of histone deacetylase [22] and enhanced neutrophil-mediated inflammation [23] in smokers. However, there is limited information on the effects of cigarette smoking on airway inflammation in asthma.…”
Section: Discussionmentioning
confidence: 98%