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Anti-inflammatory effect of adenovirus-mediated IB overexpression in respiratory epithelial cells

¹ Dept of Internal Medicine, Seoul National University College of Medicine, Chongno-Gu, Seoul, Korea. ² Clinical Research Institute, Seoul National University Hospital, Chongno-Gu, Seoul, Korea. ³ Lung Institute, Seoul National University Medical Research Center, Chongno-Gu, Seoul, Korea

CORRESPONDENCE: C.G. Yoo, Dept of Internal Medicine, Seoul National University College of Medicine, 28 Yongon-Dong, Chongno-Gu, Seoul, 110-799, Korea. Fax: 82 27629662

Keywords: adenovirus, interleukin-;8, IB super-repressor, nuclear factor-B, respiratory epithelial cells, tumour necrosis factor-;

Received: November 28, 2000
This work was supported by the 1999 National Research and Development Programme (Ministry of Science and Technology).

Many studies into basic biological characteristics of inflammation and tissue injury have implicated pro-inflammatory cytokine-mediated tissue injury in the pathogenesis of inflammatory lung diseases. Because transcription of most pro-inflammatory cytokines is dependent on the activation of nuclear factor (NF)-B, NF-B could be a good potential target to suppress the cytokine cascade. Cytokine-induced activation of NF-B requires phosphorylation and subsequent degradation of IBa. Therefore, the blocking NF-B activation by IB could inhibit the pro-inflammatory cytokine-induced tissue injury.

To evaluate whether blocking of NF-B activation shows an anti-inflammatory effect, this study investigated the effect of adenovirus-mediated overexpression of IB super-repressor (IB-SR) on the pro-inflammatory cytokine expression in respiratory epithelial cells.

The transduction efficiency of adenovirus was >90% in both A549 and NCI-H157 cells. Ad5IB-SR-transduced cells expressed high levels of IB-SR, which was resistant to tumour necrosis factor (TNF)-;-;induced degradation. Adenovirus-mediated overexpression of IB-SR blocked cytokine-induced nuclear translocation of p65 and NF-B deoxyribonucleic acid binding activity without affecting total cellular expression level of NF-B. Ad5IB-SR transduction suppressed cytokine-induced interleukin-;8 and TNF-; expressions at both ribonucleic acid and protein levels.

These results suggest that blocking the nuclear factor-B pathway by adenovirus-mediated overexpression of IB-super-repressor shows an effective anti-inflammatory effect in respiratory epithelial cells.

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