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폐상피세포에서 Dexamethasone에 의한 NF-${\kappa}B$ Transactivation 억제기전에 관한 연구
이계영,김윤섭,고미혜,박재석,지영구,김건열,곽상준,Lee, Kye-Young,Kim, Yoon-Seop,Ko, Mi-Hye,Park, Jae-Seok,Jee, Young-Koo,Kim, Keun-Youl,Kwak, Sahng-June 대한결핵및호흡기학회 2000 Tuberculosis and Respiratory Diseases Vol.48 No.5
Glucocorticoid receptor (GR) functions as a suppressor of inflammation by inhibiting the expression of many cytokine genes activated by NF-${\kappa}B$. The goal of this study is to investigate the mechanism by which GR repress NF-${\kappa}B$ activation in lung epithelial cells. We used A549 and BEAS-2B lung epithelia! cell lines. Using Ig$G{\kappa}$-NF-${\kappa}B$ luciferase reporter gene construct, we found that dexamethasone significantly suppressed TNF-$\alpha$-induced NF-${\kappa}B$ activation and the overexpression of GR showed dose-dependent reduction of TNF-$\alpha$-induced NF-${\kappa}B$ activity in both cell lines. However, DNA binding of NF-${\kappa}B$ induced by TNF-$\alpha$ in electromobility shift assay was not inhibited by dexamethasone. Super shift assay with anti-p65 antibody demonstrated the existence of p65 in NF-${\kappa}B$ complex induced by $\alpha$ Western blot showed that $I{\kappa}B{\alpha}$ degradation induced by TNF-$\alpha$ was not affected by dexamethasone and $I{\kappa}B{\kappa}$ was not induced by dexamethasone, neither. To evaluate p65 specific transactivation, we adopted co-transfection study of Gal4-p65TA1 or TA2 fusion protein expression system together with 5xGal4-luciferase vector. Co-transfection of GR with Gal4-p65TA1 or TA2 repressed luciferase activity profoundly to the level of 10-20% of p65TA1- or TA2-induced transcriptional activity. And this transrepressional effect was abolished by co-transfection of CBP of SRC-1 expression vectors. These results suggest that GR-mediated transrepression of NF-${\kappa}B$ in lung epithelial cells is through competing for binding to limiting amounts of transcriptional coactivators, CBP or SRC-1.
인체 담관 질환의 담즙에서 검출되는 Helicobacter 균주의 동정
김석배(Suk Bae Kim),이병석(Byoung Suk Lee),박태진(Tae Jin Park),고미혜(Mi Hye Ko),박현종(Hyun Jong Park),노임환(Im Hwan Roe),신지현(Ji Hyun Shin),이종화(Jong Hwa Lee) 대한내과학회 2000 대한내과학회지 Vol.58 No.5
N/A Background : Several studies have been reported that the presence of Helicobacter DNA in human bile sample, although its pathological role is not clear. The purpose of this study was to evaluate the presence and identification of Helicobacter species in human bile samples obtained from patients with biliary tract diseases. Methods : 58 bile samples (35 intrahepatic duct stones, 10 bile duct cancer, 13 pancreatic cancer) were obtained by percutaneous transhepatic biliary drainage (PTBD). DNA was isolated from bile sample. The primers were designed to amplify region of Helicobacter genus specific 16S rRNA. Polymerase chain reaction (PCR)-restriction fragment length polymorphism (RFLP) was developed to differenciate the presence of H. pylori, H. bilis, H. rappini and H. muridarum. Results : Forty-two of 58 (72.4%) bile samples obtained from patients with biliary tract disease showed positive PCR band for Helicobacter genus specific 16S rRNA. H. pylori was found in 83.3% of positive samples. Either H. bilis or H. rappini was in 16.7%. H. muridarum, however, was not detected. Conclusion : Helicobacter genus was detected in human bile samples obtained from patients with biliary tract diseases using PCR method, and the major species was H. pylori. In addition, RFLP technique was used successfully to identify Helicobacter species.(Korean J Med 58:526-531, 2000)