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논문 기본 정보

자료유형
학술저널
저자정보
Jung-Bo Yang (Chungnam National University School of Medicine) Juan-Hua Quan (The Affiliated Hospital of Guangdong Medical College) Ye-Eun Kim (Chungnam National University School of Medicine) Yun-Ee Rhee (Chungnam National University School of Medicine) Byung-Hyun Kang (Chungnam National University School of Medicine) In-Wook Choi (Chungnam National University School of Medicine) Guang-Ho Cha (Chungnam National University School of Medicine) Jae-Min Yuk (Chungnam National University School of Medicine) Young-Ha Lee (Chungnam National University School of Medicine)
저널정보
대한기생충학열대의학회 Parasites, Hosts and Diseases The Korean Journal of Parasitology Vol.53 No.4
발행연도
2015.8
수록면
371 - 377 (7page)

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Trichomonas vaginalis induces proinflammation in cervicovaginal mucosal epithelium. To investigate the signaling pathways in TNF-α production in cervical mucosal epithelium after T. vaginalis infection, the phosphorylation of PI3K/AKT and MAPK pathways were evaluated in T. vaginalis-infected SiHa cells in the presence and absence of specific inhibitors. T. vaginalis increased TNF-α production in SiHa cells, in a parasite burden-dependent and incubation time-dependent manner. In T. vaginalis-infected SiHa cells, AKT, ERK1/2, p38 MAPK, and JNK were phosphorylated from 1 hr after infection; however, the phosphorylation patterns were different from each other. After pretreatment with inhibitors of the PI3K/AKT and MAPK pathways, TNF-α production was significantly decreased compared to the control; however, TNF-α reduction patterns were different depending on the type of PI3K/MAPK inhibitors. TNF-α production was reduced in a dose-dependent manner by treatment with wortmannin and PD98059, whereas it was increased by SP600125. These data suggested that PI3K/AKT and MAPK signaling pathways are important in regulation of TNF-α production in cervical mucosal epithelial SiHa cells. However, activation patterns of each pathway were different from the types of PI3K/MAPK pathways.

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Abstract
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES

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UCI(KEPA) : I410-ECN-0101-2016-513-001839404