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어류병원균 Streptococcus iniae의 toxin/antitoxin system에 대한 연구
윤성용(Seongyong Yoon),김연하(Yeon Ha Kim),전문정(Moonjung Jeun),성민지(Minji Seong),유아영(Ah Young Yoo),이동희(Donghee Lee),문기환(Ki Hwan Moon),강호영(Ho Young Kang) 한국생명과학회 2019 생명과학회지 Vol.29 No.1
Streptococcus iniae는 대표적인 어류병원균으로 인수공통의 질병을 일으킨다. S. iniae FP5228에 존재하는 병원성 인자를 찾고자 하는 연구과정에서 S. iniae를 24시간 이상 배양한 배양액에는 살아있는 균의 수가 급격하게 감소하는 현상을 발견하였다. 이 현상은 FP5228 균이 가지고 있는 14 kb plasmid 상에 있는 toxin/antitoxin (TA) system의 구성요소인 toxin ζ와 antitoxin ε 유전자가 관련이 있을 것이란 가설을 설정하였다. IPTG와 arabinose에 의해 toxin ζ와 antitoxin ε의 발현이 조절되는 pBP1140 vector system을 구축하였다. E. coli/pBP1140 균주는 toxin이 발현되는 조건에서 초기 생육이 느려졌고, 현미경의 관찰에서 균체가 길어짐을 확인하였다. FP5228 균주가 가진 14 kb plasmid를 없앤 S. iniae CK287을 제조하였다. CK287 균은 배양 중 급격하게 사멸되는 현상을 보이지 않았고, biofilm 생성능력도 감소하였고 세포독성 시험과 물고기 시험에서 독성이 약화 된 것이 확인되었다. 이들 결과들은 TA system이 생리적 조절 및 병원성 인자의 발현에 관련이 있음을 추정할 수 있다. Streptococcus iniae is a typical fish pathogen causing streptococcosis and it can also cause zoonotic infectious diseases. We studied S. iniae FP5228 isolated from infected olive flounder in Wando, Korea. In a study to find virulence factors in FP5228, we found that the number of live bacteria decreased dramatically in culture medium containing S. iniae FP5228 for more than 24 hr. This phenomenon was hypothesized to be related to Toxin ζ and Antitoxin ε genes, components of the Toxin/ Antitoxin (TA) system on the 14 kb plasmid of FP5228. We used a protein overexpression system to identify it. The pBP1140 vector system was constructed to regulate the expression of Toxin ζ and Antitoxin ε by IPTG and Arabinose. E. coli/pBP1140 strain grew slowly in early growth under toxin expression condition, and it was confirmed by microscopic observation that the strain became longer. S. iniae CK287, lacking a 14 kb plasmid of S. iniae FP5228 strain, was constructed. CK287 bacterial cells did not show rapid killing during culture, and the ability to produce biofilm was also decreased, and toxicity was weakened in cytotoxicity test and fish test. These results suggest that the TA system is involved in physiological regulation and expression of virulence factors in S. iniae FP5228.
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Propofol Suppresses LPS-Induced Inflammation in Amnion Cells via Inhibition of NF-κB Activation
Ji-Young Yoon,Do-Wan Kim,Ji-Hye Ahn,Eun-Ji Choi,Yeon Ha Kim,전문정,김은정 한국조직공학과 재생의학회 2019 조직공학과 재생의학 Vol.16 No.3
BACKGROUND: Preterm labor is a leading risk factor for neonatal death and long-term impairment and linked closely with inflammation. Non-obstetric surgery is occasionally needed during pregnancy and the anesthetic drugs or surgery itself can give rise to inflammation. Here, we examined the influence of propofol pretreatment on the expression of cyclooxygenase-2 (COX-2) and prostaglandin E2 (PGE2) after lipopolysaccharide (LPS) stimulation. In addition, we evaluated the expression of pro-inflammatory cytokines and nuclear factor kappa B (NF-jB). METHODS: Human amnion-derived WISH cells were used to investigate the effect of propofol on the LPS-induced expression of inflammatory substances involved in preterm labor. For the experiment, WISH cells were pretreated with various concentrations propofol (0.01–10 lg/ml) for 1 h and then treated with LPS (1 lg/ml) for 24 h. Cytotoxicity was evaluated using MTT assay. PGE2 concentration was assessed by ELISA. Protein expressions of COX-2, PGE2 and NF-jB were analyzed by western blotting analysis. RT-PCR was used for analysis of mRNA expression of COX-2, PGE2, interlukin (IL)-1b and tumor necrosis factor (TNF)-a. RESULTS: Propofol showed no cytotoxicity on the WISH cells. LPS-induced PGE2 production and COX-2 and PGE2 expression were decreased after propofol pretreatment. Propofol also attenuated the LPS-induced mRNA expression of IL- 1b and TNF-a. Moreover, the activation of NF-jB was inhibited by propofol pretreatment on LPS-stimulated WISH cells. CONCLUSION: We demonstrated that propofol suppresses the expression of inflammatory substances enhanced by LPS stimulation. Furthermore, this inhibitory effect of propofol on the inflammatory substance expression is mediated by suppression of NF-jB activation.
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