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Am J Physiol Lung Cell Mol Physiol 280: L3-L9, 2001;
1040-0605/01 $5.00
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Vol. 280, Issue 1, L3-L9, January 2001

Effect of acetylsalicylic acid on endogenous Ikappa B kinase activity in lung epithelial cells

Chul-Gyu Yoo1,2,3, Seunghee Lee1,2, Choon-Taek Lee1,2,3, Young Whan Kim1,2,3, Sung Koo Han1,2,3, and Young-Soo Shim1,2,3

1 Department of Internal Medicine, Seoul National University College of Medicine, and 3 Lung Institute, Seoul National University Medical Research Center, Chongno-Gu, Seoul 110-799; and 2 Clinical Research Institute, Seoul National University Hospital, Chongno-Gu, Seoul 110-744, Korea

The anti-inflammatory effect of acetylsalicylic acid (ASA) has been thought to be secondary to the inhibition of prostaglandin synthesis. Because doses of ASA necessary to treat chronic inflammatory diseases are much higher than those needed to inhibit prostaglandin synthesis, a prostaglandin-independent pathway has been emerging as the new anti-inflammatory mechanism of ASA. Here, we examined the effect of ASA on the interleukin (IL)-1beta - and tumor necrosis factor (TNF)-alpha -induced proinflammatory cytokine expression and evaluated whether this effect is closely linked to the nuclear factor (NF)-kappa B/Ikappa B-alpha pathway. A high dose of ASA blocked IL-1beta - and TNF-alpha -induced TNF-alpha and IL-8 expression, respectively. ASA inhibited TNF-alpha -induced activation of NF-kappa B by preventing phosphorylation and subsequent degradation of Ikappa B-alpha in a prostanoid-independent manner. TNF-alpha -induced activation of Ikappa B kinase was also suppressed by ASA pretreatment. These observations suggest that the anti-inflammatory effect of ASA in lung epithelial cells may be due to suppression of Ikappa B kinase activity, which thereby inhibits subsequent phosphorylation and degradation of Ikappa B-alpha , activation of NF-kappa B, and proinflammatory cytokine expression in lung epithelial cells.

nuclear factor-kappa B; interleukin-8


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