Involvement of PI3K/AKT and MAPK Pathways for TNF-α Production in SiHa Cervical Mucosal Epithelial Cells Infected with Trichomonas vaginalis.
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.
Department of Obstetrics and Gynecology, Chungnam National University School of Medicine, Daejeon 301-131, Korea.
Jung-Bo
JB
Yang
Department of Gastroenterology, The Affiliated Hospital of Guangdong Medical College, Zhanjiang 524-001, Guangdong, China.
Juan-Hua
JH
Quan
Department of Biomedical Science, Chungnam National University School of Medicine, Daejeon 301-131, Korea.
Ye-Eun
YE
Kim
Department of Obstetrics and Gynecology, Chungnam National University School of Medicine, Daejeon 301-131, Korea.
Yun-Ee
YE
Rhee
Department of Obstetrics and Gynecology, Chungnam National University School of Medicine, Daejeon 301-131, Korea.
Byung-Hyun
BH
Kang
Department of Infection Biology, Chungnam National University School of Medicine, Daejeon 301-131, Korea.
In-Wook
IW
Choi
Department of Infection Biology, Chungnam National University School of Medicine, Daejeon 301-131, Korea.
Guang-Ho
GH
Cha
Department of Infection Biology, Chungnam National University School of Medicine, Daejeon 301-131, Korea.
Jae-Min
JM
Yuk
Department of Infection Biology, Chungnam National University School of Medicine, Daejeon 301-131, Korea.
Young-Ha
YH
Lee
D002460:Cell Line; D002584:Cervix Uteri / Q000201:enzymology / Q000378:metabolism / Q000469:parasitology*; D004847:Epithelial Cells / Q000201:enzymology* / Q000378:metabolism / Q000469:parasitology; D005260:Female; D006801:Humans; D020935:MAP Kinase Signaling System; D009092:Mucous Membrane / Q000201:enzymology* / Q000378:metabolism / Q000469:parasitology; D019869:Phosphatidylinositol 3-Kinases / Q000235:genetics / Q000378:metabolism*; D051057:Proto-Oncogene Proteins c-akt / Q000235:genetics / Q000378:metabolism*; D014247:Trichomonas Vaginitis / Q000201:enzymology* / Q000235:genetics / Q000378:metabolism / Q000469:parasitology; D014246:Trichomonas vaginalis / Q000502:physiology*; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism*
D014409:Tumor Necrosis Factor-alpha; D019869:Phosphatidylinositol 3-Kinases; D051057:Proto-Oncogene Proteins c-akt
MAPK; PI3K/AKT; SiHa cell; TNF-α; Trichomonas vaginalis