Increased intracellular Cl− concentration mediates Trichomonas vaginalis-induced inflammation in the human vaginal epithelium

Xu, Jian-Bang; Zhang, Yilin; Huang, Jiehong; Lu, Shen-Jiao; Sun, Qing; Chen, Peng-Xiao; Jiang, Ping; Qiu, Zhen; Jiang, Funeng; Zhu, Yun-Xin; Lai, De‐Hua; Zhong, Weijie; Lun, Zhao‐Rong; Zhou, Wen‐Liang

doi:10.1016/j.ijpara.2019.04.005

Cited by 8 publications

(15 citation statements)

References 60 publications

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“…Furthermore, we also evaluate the effect of T. vaginalis infection on CFTR function using the intracellular Cl − measurement technique. Treatment with CFTR inh-172 (10 μM) elicited a decrease of MQAE fluorescence in the primary cultured rat vaginal epithelial cells, which represented an increase of intracellular Cl − concentration owing to the dysfunction of CFTR as described previously [30]. Nevertheless, the decrease of MQAE fluorescence elicited by CFTR inh-172 was significantly restrained after T. vaginalis infection (Fig 3E -3G), indicating that T. vaginalis impaired the Cl − transport function of CFTR in rat vaginal epithelial cells.…”

Section: T Vaginalis Infection Triggered Down-regulation Of Cftr In supporting

confidence: 55%

“…T. vaginalis strain CPO 02 was obtained as a kind gift from Prof. Zhao-Rong Lun (School of Life Sciences, Sun Yat-sen University, Guangzhou, China), and was cultured as previously described [30]. Briefly, the T. vaginalis trophozoites were cultured in Diamond's Trypticase Yeast Extract Maltose (TYM) medium (Huankai Microbial, China), supplemented with 10% (vol/vol) heat-inactivated fetal bovine serum (FBS, Tianhang Biotechnology, China), penicillin/streptomycin (100 U/mL/100 μg/mL, Hyclone, USA) at 37˚C in an atmosphere of 5% CO 2 [31].…”

Section: Parasites and Animalsmentioning

confidence: 99%

“…Western blot was performed as described previously [30]. The primary antibody against CFTR (1:500, ab2784) was purchased from Abcam (UK), and the antibody against β-actin (1:1000, #4970) was purchased from Cell Signalling Technology (USA).…”

Section: Western Blotmentioning

confidence: 99%

“…The measurement of intracellular Cl − was performed as previously described [30]. Briefly, the primary cultured rat vaginal epithelial cells or the VK2/E6E7 cells were grown on glass cover slips with or without T. vaginalis infection for 3 h. The changes of fluorescence intensity of the Cl − indicator dye, MQAE, was recorded using an imaging system (Olympus, IX83, Tokyo, Japan).…”

Section: Intracellular CL − Measurementmentioning

confidence: 99%

“…epithelial Cl − secretion mediated by CFTR, suggesting a close correlation between pathogen infection and aberrant function of CFTR in host epithelial cells. As the prerequisite to colonization, T. vaginalis adheres to the host vaginal epithelial cells and initiates the inflammatory response [18,23,29,30]. Our previous work has revealed that in human vaginal epithelial cells, T. vaginalis infection elicited the down-regulation of CFTR in a cysteine protease-dependent manner, thereby mediating epithelial inflammation via intracellular Cl − signaling pathways [30].…”

Section: Introductionmentioning

confidence: 99%

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Trichomonas vaginalis infection impairs anion secretion in vaginal epithelium

et al. 2021

PLoS Negl Trop Dis

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Trichomonas vaginalis is a common protozoan parasite, which causes trichomoniasis associated with severe adverse reproductive outcomes. However, the underlying pathogenesis has not been fully understood. As the first line of defense against invading pathogens, the vaginal epithelial cells are highly responsive to environmental stimuli and contribute to the formation of the optimal luminal fluid microenvironment. The cystic fibrosis transmembrane conductance regulator (CFTR), an anion channel widely distributed at the apical membrane of epithelial cells, plays a crucial role in mediating the secretion of Cl− and HCO3−. In this study, we investigated the effect of T. vaginalis on vaginal epithelial ion transport elicited by prostaglandin E2 (PGE2), a major prostaglandin in the semen. Luminal administration of PGE2 triggered a remarkable and sustained increase of short-circuit current (ISC) in rat vaginal epithelium, which was mainly due to Cl− and HCO3− secretion mediated by the cAMP-activated CFTR. However, T. vaginalis infection significantly abrogated the ISC response evoked by PGE2, indicating impaired transepithelial anion transport via CFTR. Using a primary cell culture system of rat vaginal epithelium and a human vaginal epithelial cell line, we demonstrated that the expression of CFTR was significantly down-regulated after T. vaginalis infection. In addition, defective Cl− transport function of CFTR was observed in T. vaginalis-infected cells by measuring intracellular Cl− signals. Conclusively, T. vaginalis restrained exogenous PGE2-induced anion secretion through down-regulation of CFTR in vaginal epithelium. These results provide novel insights into the intervention of reproductive complications associated with T. vaginalis infection such as infertility and disequilibrium in vaginal fluid microenvironment.

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Section: T Vaginalis Infection Triggered Down-regulation Of Cftr In supporting

confidence: 55%

Section: Parasites and Animalsmentioning

confidence: 99%

Section: Western Blotmentioning

confidence: 99%

Section: Intracellular CL − Measurementmentioning

confidence: 99%