Korean J Parasitol.  2015 Aug;53(4):371-377. 10.3347/kjp.2015.53.4.371.

Involvement of PI3K/AKT and MAPK Pathways for TNF-alpha Production in SiHa Cervical Mucosal Epithelial Cells Infected with Trichomonas vaginalis

  • 1Department of Obstetrics and Gynecology, Chungnam National University School of Medicine, Daejeon 301-131, Korea.
  • 2Department of Gastroenterology, The Affiliated Hospital of Guangdong Medical College, Zhanjiang 524-001, Guangdong, China.
  • 3Department of Biomedical Science, Chungnam National University School of Medicine, Daejeon 301-131, Korea.
  • 4Department of Infection Biology, Chungnam National University School of Medicine, Daejeon 301-131, Korea. yhalee@cnu.ac.kr


Trichomonas vaginalis induces proinflammation in cervicovaginal mucosal epithelium. To investigate the signaling pathways in TNF-alpha 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-alpha 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-alpha production was significantly decreased compared to the control; however, TNF-alpha reduction patterns were different depending on the type of PI3K/MAPK inhibitors. TNF-alpha 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-alpha production in cervical mucosal epithelial SiHa cells. However, activation patterns of each pathway were different from the types of PI3K/MAPK pathways.


Trichomonas vaginalis; SiHa cell; PI3K/AKT; MAPK; TNF-alpha
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