ArticleThe Korean journal of parasitology2016
Inflammatory Responses in a Benign Prostatic Hyperplasia Epithelial Cell Line (BPH-1) Infected with Trichomonas vaginalis.
Article in The Korean journal of parasitology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 25 citations in OpenAlex.
- Investigating the impact of gut microbiota-derived metabolites on benign prostatic hyperplasia using network pharmacology approaches.BMC pharmacology & toxicology · 2026Article
- Recent Advances in Biology, Host and Microbe Interactions of the Human Sexually Transmitted ParasiteInternational journal of molecular sciences · 2025Review
- Intrinsic and extrinsic factors causing hyperplasia of the prostate.International journal of urology : official journal of the Japanese Urological Association · 2024Review
- P. gingivalis in oral-prostate axis exacerbates benign prostatic hyperplasia via IL-6/IL-6R pathway.Military Medical Research · 2024Article
- Trichomoniasis.Infectious disease clinics of North America · 2023Review
- Efficacy of Buzhong Yiqi decoction on benign prostatic hyperplasia and its possible mechanism.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2023Article
- Infinity war:Microbial cell (Graz, Austria) · 2023Review
- The correlation between Trichomonas vaginalis infection and reproductive system cancer: a systematic review and meta-analysis.Infectious agents and cancer · 2023Article
- Inflammatory response to Trichomonas vaginalis in the pathogenesis of prostatitis and benign prostatic hyperplasia.Parasites, hosts and diseases · 2023Review
- Association between trichomoniasis and prostate and bladder diseases: a population-based case-control study.Scientific reports · 2022Article
- Ellagic acid improves benign prostate hyperplasia by regulating androgen signaling and STAT3.Cell death & disease · 2022Article
- IL-6 Signaling Link between Inflammatory Tumor Microenvironment and Prostatic Tumorigenesis.Analytical cellular pathology (Amsterdam) · 2022Review
- Development of a convenient detection method for Trichomonas vaginalis based on loop-mediated isothermal amplification targeting adhesion protein 65.BMC infectious diseases · 2020Article
- Atractylenolide II Induces Apoptosis of Prostate Cancer Cells through Regulation of AR and JAK2/STAT3 Signaling Pathways.Molecules (Basel, Switzerland) · 2018Article
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Authors and funding
5 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Trichomonas vaginalis causes the most prevalent sexually transmitted infection worldwide. Trichomonads have been detected in prostatic tissues from prostatitis, benign prostatic hyperplasia (BPH), and prostate cancer. Chronic prostatic inflammation is known as a risk factor for prostate enlargement, benign prostatic hyperplasia symptoms, and acute urinary retention. Our aim was to investigate whether T. vaginalis could induce inflammatory responses in cells of a benign prostatic hyperplasia epithelial cell line (BPH-1). When BPH-1 cells were infected with T. vaginalis, the protein and mRNA of inflammatory cytokines, such as CXCL8, CCL2, IL-1β, and IL-6, were increased. The activities of TLR4, ROS, MAPK, JAK2/STAT3, and NF-κB were also increased, whereas inhibitors of ROS, MAPK, PI3K, NF-κB, and anti-TLR4 antibody decreased the production of the 4 cytokines although the extent of inhibition differed. However, a JAK2 inhibitor inhibited only IL-6 production. Culture supernatants of the BPH-1 cells that had been incubated with live T. vaginalis (trichomonad-conditioned medium, TCM) contained the 4 cytokines and induced the migration of human monocytes (THP-1 cells) and mast cells (HMC-1 cells). TCM conditioned by BPH-1 cells pretreated with NF-κB inhibitor showed decreased levels of cytokines and induced less migration. Therefore, it is suggested that these cytokines are involved in migration of inflammatory cells. These results suggest that T. vaginalis infection of BPH patients may cause inflammation, which may induce lower urinary tract symptoms (LUTS).
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