Tuberc Respir Dis > Volume 49(3); 2000 > Article
Tuberculosis and Respiratory Diseases 2000;49(3):332-342.
DOI:    Published online September 1, 2000.
Pro-inflammatory cytokine expression through NF-kappaB/IkappaB pathway in lung epithelial cells.
Gye Young Park, Seung Hee Lee, Bin Hwangbo, Jae Joon Yim, Choon Taek Lee, Young Whan Kim, Sung Koo Han, Young Soo Shim, Chul Gyu Yoo
The importance of pro-inflammatory cytokines, especially tumor necrosis factor α(TNF-α) and interleukin-1β(IL-1β), have been extensively documented in the generation of inflammatory lung disease. Lung epithelial cells are also actively involved in initiating and maintaining inflammation by producing pro-inflammatory mediators. Understanding the mechanism of pro-inflammatory cytokine expression in lung epithelial cells is crucial to the development of new therapeutic modalities for inflammatory lung disease. Transcription of most pro-inflammatory cytokines is dependent on the actiation of NF-κB. However, the relationship between pro-inflammatory cytokine expression and NF-κB/IκB pathway in lung epithelial cells is not clear. METHODS: BEAS-2B, A549, NCI-H719 cells were stimulated with IL-1β or TNF-α at various times, and then IL-8 and TNF-αmRNA expressions were assayed by Northern blot analysis. IL-1β or TNF-α-induced NF-κB activation was assessed by the nuclear translocation of p65 NF-κB subunit. The degradation of IκBα and IκBβ by IL-1βor TNF-α stimulation was assayed by Western blot analysis. The phosphorylation of IκBαwas evaluated by Western blot analysis after pre-treating cells with proteasome inhibitor followed by IL-1β or TNF-α stimulation. The basal level of IKKα expression was evaluated by Western blot analysis. RESULTS: IκBαand IκBβ was repidly degraded after 5 minutes of incubation with IL-1β or TNF-α in BEAS-2B, A549, and NCI-H157 cells. The activation of NF-κB and the induction of IL-8 and TNF-α mRNA expressions were observed by IL-1β or TNF-α stimulation in these cells. In contrast, neither the changes in NF-κB/IκB pathway nor IL-8 and TNF-α mRNA expression was induces by IL-1β or TNF-α stimulation in NCI-H719 cell. IL-1β and TNF-α-induced IκB phoshorylation was observed in BEAS-2B, A549, and NCI-H157 cells, but not in NCI-H719 cells. The basal level of IKKα expression was not different between cells. CONCLUSION: NF-κB/IκB pathway plays an important role in the ixpression of pro-inflammatory cytokine in most lung epithelial cells. The absence of the effect on NF-κB/IκB pathway in NCI-H719 cells seems to be due to the defect in the intracellular signal transduction pathway upstream to IKK.
Key Words: NF-κB, IκBα, Lung epithelial cells, Pro-inflammatory cytokine

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