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BioMed Research International
Volume 2017, Article ID 3904870, 10 pages
https://doi.org/10.1155/2017/3904870
Research Article

Trichomonas vaginalis Induces SiHa Cell Apoptosis by NF-κB Inactivation via Reactive Oxygen Species

1Department of Gastroenterology, Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong Province 524001, China
2Department of Obstetrics and Gynecology, Chungnam National University School of Medicine, Daejeon 35015, Republic of Korea
3Department of Infection Biology, Chungnam National University School of Medicine, Daejeon 35015, Republic of Korea

Correspondence should be addressed to Young-Ha Lee; rk.ca.unc@eelahy

Received 18 August 2017; Revised 7 November 2017; Accepted 19 November 2017; Published 18 December 2017

Academic Editor: Marlene Benchimol

Copyright © 2017 Juan-Hua Quan et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Trichomonas vaginalis induces apoptosis in host cells through various mechanisms; however, little is known about the relationship between apoptosis, reactive oxygen species (ROS), and NF-κB signaling pathways in the cervical mucosal epithelium. Here, we evaluated apoptotic events, ROS production, and NF-κB activity in T. vaginalis-treated cervical mucosal epithelial SiHa cells, with or without specific inhibitors, using fluorescence microscopy, DNA fragmentation assays, subcellular fractionation, western blotting, and luciferase reporter assay. SiHa cells treated with live T. vaginalis at a multiplicity of infection of 5 (MOI 5) for 4 h produced intracellular and mitochondrial ROS in a parasite-load-dependent manner. Incubation with T. vaginalis caused DNA fragmentation, cleavage of caspase 3 and PARP, and release of cytochrome c into the cytoplasm. T. vaginalis-treated SiHa cells showed transient early NF-B p65 nuclear translocation, which dramatically dropped at 4 h after treatment. Suppression of NF-κB activity was dependent on parasite burden. However, treatment with the ROS scavenger, N-acetyl-C-cysteine (NAC), reversed the effect of T. vaginalis on apoptosis and NF-κB inactivation in SiHa cells. Taken together, T. vaginalis induces apoptosis in human cervical mucosal epithelial cells by parasite-dose-dependent ROS production through an NF-κB-regulated, mitochondria-mediated pathway.