RESEARCH - Cigarette smoke condensate upregulates the gene and protein expression of proinflammatory cytokines in human fibroblast-like synoviocyte line

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J Interferon Cytokine Res. 2008 Aug;28(8):509-21.

Cigarette smoke condensate upregulates the gene and protein expression

of proinflammatory cytokines in human fibroblast-like synoviocyte

line.

Shizu M, Itoh Y, Sunahara R, Chujo S, Hayashi H, Ide Y, Takii T,

Koshiko M, Chung SW, Hayakawa K, Miyazawa K, Hirose K, Onozaki K.

Department of Molecular Health Sciences, Graduate School of

Pharmaceutical Sciences, Nagoya City University, Mizuho, Nagoya,

Japan.

Rheumatoid arthritis (RA) is characterized by proliferation of

synoviocytes that produce proinflammatory cytokines, which are

implicated in the pathogenesis of RA. When human fibroblast-like

synoviocytes line MH7A was treated with cigarette smoke condensate

(CSC), either mainstream or sidestream, expression levels of

interleukin (IL)-1alpha, IL-1beta, IL-6, IL-8, and CYP1A1 mRNA were

upregulated in both time- and dose-dependent manners. The upregulatory

effects of CSC on these cytokines were not significantly inhibited by

alpha-naphthoflavone, an aryl hydrocarbon receptor (AhR) antagonist,

suggesting that the effects of CSC were independent of AhR.

Cycloheximide treatment indicated that the augmenting effect of CSC on

IL-1alpha, IL-1beta and IL-8, but not IL-6 and CYP1A1, mRNA expression

requires de novo protein synthesis. CSC also induced cytokines at

protein levels and further augmented the effects of tumor necrosis

factor alpha on induction of these cytokines at both mRNA and protein

levels.

These results support the epidemiological studies indicating a strong

association between heavy cigarette smoking and pathogenesis of RA.

PMID: 18729741

http://www.ncbi.nlm.nih.gov/pubmed/18729741

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