Involvement of PI3K/AKT and MAPK Pathways for TNF-α Production in SiHa Cervical Mucosal Epithelial Cells Infected with Trichomonas vaginalis
2
조회
0
다운로드
0
인용
0
참고문헌
키워드
초록
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.
Abstract
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.
참고문헌 (23)
- Johnston VJ, "Global epidemiology and control of Trichomonas vaginalis", Curr Opin Infect Dis, 21, pp.56~64 (2008)
- Ryan CM, "Trichomonas vaginalis: current understanding of host-parasite interactions", Essays Biochem, 51, pp.161~175 (2011)
- Van der Pol B, "Trichomonas vaginalis infection: the most prevalent nonviral sexually transmitted infection receives the least public health attention", Clin Infect Dis, 44, pp.23~25 (2007)
- Coleman JS, "Trichomonas vaginalis vaginitis in obstetrics and gynecology practice: new concepts and controversies", Obstet Gynecol Surv, 68, pp.43~50 (2013)
- Guenthner PC, "Trichomonas vaginalis-induced epithelial monolayer disruption and human immunodeficiency virus type 1 (HIV-1) replication: implications for the sexual transmission of HIV-1", Infect Immun, 73, pp.4155~4160 (2005)
- Quayle AJ, "The innate and early immune response to pathogen challenge in the female genital tract and the pivotal role of epithelial cells", J Reprod Immunol, 57, pp.61~79 (2002)
- Wira CR, "Epithelial cells in the female reproductive tract: a central role as sentinels of immune protection", Am J Reprod Immunol, 53, pp.65~76 (2005)
- Cole AM, "Innate host defense of human vaginal and cervical mucosae", Curr Top Microbiol Immunol, 306, pp.199~230 (2006)
- Malla N, "Kinetics of serum and local cytokine profile in experimental intravaginal trichomoniasis induced with Trichomonas vaginalis isolates from symptomatic and asymptomatic women", Parasite Immunol, 29, pp.101~105 (2007)
- Aksamitiene E, "Cross-talk between mitogenic Ras", MAPK and survival PI3K, Biochem Soc Trans, pp.2012, 40[DOI]
- Yang ZZ, "Physiological functions of protein kinase B", Akt, 2004, pp.32, 350~354
- Gasparini C, "NF-κB as a target for modulating inflammatory responses", Curr Pharm, 18, pp.5735~5745 (2012)
- Cargnello M, "Activation and function of the MAPKs and their substrates, the MAPK-activated protein kinases", Microbiol Mol Biol Rev, 75, pp.50~83 (2011)
- Paintlia MK, "Specific IgA response, T-cell subtype and cytokine profile in experimental intravaginal trichomoniasis", Parasitol Res, 88, pp.338~343 (2002)
- Lin MC, "The antimicrobial peptide, shrimp anti-lipopolysaccharide factor (SALF), inhibits proinflammatory cytokine expressions through the MAPK and NF-κB pathways in Trichomonas vaginalis adherent to HeLa cells", Peptides, 38, pp.197~207 (2012)
- Eun-Ju Chang, "Trichomonas vaginalis Inhibits Proinflammatory Cytokine Production in Macrophages by Suppressing NF-kB Activation", Molecules and Cells, 18(2), pp.177~185 (2004), 한국분자세포생물학회
- Ik-Hwan Han, "Proinflammatory Cytokine and Nitric Oxide Production by Human Macrophages Stimulated with Trichomonas vaginalis", The Korean Journal of Parasitology, 47(3), pp.205~212 (2009), 대한기생충학ㆍ열대의학회
- Aggarwal BB, "The role of TNF and its family members in inflammation and cancer: lessons from gene deletion", Curr Drug Targets Inflamm Allergy, 1, pp.327~341 (2002)
- Quan JH, "Trichonomas vaginalis metalloproteinase induces apoptosis of SiHa cells through disrupting the Mcl-1", Bim and Bcl-xL, PLoS One, pp.2014, 9[DOI]
- Juan-Hua Quan, "Trichomonas vaginalis metalloproteinase induces mTOR cleavage of SiHa cells", The Korean Journal of Parasitology, 52(6), pp.595~603 (2014), 대한기생충학ㆍ열대의학회[DOI]
- 양용석, "Involvement of MAP Kinases in Apoptosis of Macrophage Treated with Trichomonas vaginalis", Yonsei Medical Journal, 45(4), pp.751~754 (2004), 연세대학교의과대학
- Zhou Z, "Role of NF-kappaB and PI 3-kinase", Akt in TNF-alpha-induced cytotoxicity in microvascular endothelial cells, 2008, pp.295, F932~F941
- Tang F, "The absence of NF-κB-mediated inhibition of c-Jun N-terminal kinase activation contributes to tumor necrosis factor alpha-induced apoptosis", Mol Cell Biol, 22, pp.8571~8579 (2002)