{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,12]],"date-time":"2025-10-12T20:03:34Z","timestamp":1760299414252},"reference-count":56,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2016,10,4]],"date-time":"2016-10-04T00:00:00Z","timestamp":1475539200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100003725","name":"National Research Foundation of Korea","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100003725","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Parasite Immunology"],"published-print":{"date-parts":[[2016,11]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p><jats:italic>Trichomonas vaginalis (Tv)<\/jats:italic> has been found in patient tissue of benign prostatic hyperplasia (<jats:styled-content style=\"fixed-case\">BPH<\/jats:styled-content>), and suggested to cause chronic prostatitis. <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20106 is known as one of the important factors of chronic inflammation in prostate cancer. Patients with chronic prostatitis\/chronic pelvic pain syndrome (<jats:styled-content style=\"fixed-case\">CP<\/jats:styled-content>\/<jats:styled-content style=\"fixed-case\">CPPS<\/jats:styled-content>) had higher levels of <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20106 in seminal plasma. Furthermore, inflammatory conditions induced by pathogen infections have been shown to promote epithelial\u2013mesenchymal transition (<jats:styled-content style=\"fixed-case\">EMT<\/jats:styled-content>). Here, we investigated the signals involved in <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20106 production by human prostate epithelial cells (<jats:styled-content style=\"fixed-case\">PEC<\/jats:styled-content>s) stimulated with <jats:italic>Tv<\/jats:italic> and examined whether <jats:italic>Tv<\/jats:italic> induces <jats:styled-content style=\"fixed-case\">EMT<\/jats:styled-content> in <jats:styled-content style=\"fixed-case\">PEC<\/jats:styled-content>s. We found that <jats:styled-content style=\"fixed-case\">PEC<\/jats:styled-content>s stimulated with <jats:italic>Tv<\/jats:italic> increased the production of <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20106, as well as the expression of <jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content>2, <jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content>4, <jats:styled-content style=\"fixed-case\">MAPK<\/jats:styled-content>s (p38, <jats:styled-content style=\"fixed-case\">JNK<\/jats:styled-content>,<jats:styled-content style=\"fixed-case\"> ERK<\/jats:styled-content>), <jats:styled-content style=\"fixed-case\">NF<\/jats:styled-content>\u2010\u03baB and <jats:styled-content style=\"fixed-case\">JAK<\/jats:styled-content>2\/<jats:styled-content style=\"fixed-case\">STAT<\/jats:styled-content>3, and levels of <jats:styled-content style=\"fixed-case\">ROS<\/jats:styled-content>. Inhibition of <jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content>2 or <jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content>4 reduced <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20106 production as well as expression of these other factors, and agents inhibiting <jats:styled-content style=\"fixed-case\">ROS<\/jats:styled-content>,<jats:styled-content style=\"fixed-case\"> MAPK<\/jats:styled-content>s, <jats:styled-content style=\"fixed-case\">NF<\/jats:styled-content>\u2010\u03baB and <jats:styled-content style=\"fixed-case\">JAK<\/jats:styled-content> reduced <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20106 production. However, when <jats:styled-content style=\"fixed-case\">PEC<\/jats:styled-content>s were stimulated with <jats:italic>Tv<\/jats:italic>, transcripts of mesenchymal cell markers increased, and epithelial cell markers decreased. In addition, the induction of <jats:styled-content style=\"fixed-case\">EMT<\/jats:styled-content> was suppressed by inhibitors of <jats:styled-content style=\"fixed-case\">JAK<\/jats:styled-content> or <jats:styled-content style=\"fixed-case\">NF<\/jats:styled-content>\u2010\u03baB. These findings are the first evidence that <jats:italic>Tv<\/jats:italic> infection of prostate epithelial cells may induce <jats:styled-content style=\"fixed-case\">EMT<\/jats:styled-content>.<\/jats:p>","DOI":"10.1111\/pim.12357","type":"journal-article","created":{"date-parts":[[2016,8,20]],"date-time":"2016-08-20T14:22:48Z","timestamp":1471702968000},"page":"678-687","source":"Crossref","is-referenced-by-count":33,"title":["Signalling pathways associated with <scp>IL<\/scp>\u20106 production and epithelial\u2013mesenchymal transition induction in prostate epithelial cells stimulated with <i>Trichomonas vaginalis<\/i>"],"prefix":"10.1111","volume":"38","author":[{"given":"I. H.","family":"Han","sequence":"first","affiliation":[{"name":"Department of Environmental Biology and Medical Parasitology Hanyang University College of Medicine  Seoul Korea"},{"name":"Department of Biomedical Science Graduate School of Biomedical Science and Engineering Hanyang University  Seoul Korea"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"J. H.","family":"Kim","sequence":"additional","affiliation":[{"name":"Department of Environmental Biology and Medical Parasitology Hanyang University College of Medicine  Seoul Korea"},{"name":"Department of Biomedical Science Graduate School of Biomedical Science and Engineering Hanyang University  Seoul Korea"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"S. S.","family":"Kim","sequence":"additional","affiliation":[{"name":"Department of Environmental Biology and Medical Parasitology Hanyang University College of Medicine  Seoul Korea"},{"name":"Department of Biomedical Science Graduate School of Biomedical Science and Engineering Hanyang University  Seoul Korea"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M. H.","family":"Ahn","sequence":"additional","affiliation":[{"name":"Department of Environmental Biology and Medical Parasitology Hanyang University College of Medicine  Seoul Korea"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"J. S.","family":"Ryu","sequence":"additional","affiliation":[{"name":"Department of Environmental Biology and Medical Parasitology Hanyang University College of Medicine  Seoul Korea"},{"name":"Department of Biomedical Science Graduate School of Biomedical Science and Engineering Hanyang University  Seoul Korea"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2016,10,4]]},"reference":[{"key":"e_1_2_7_2_1","volume-title":"Prevalence and Incidence of Selected Sexually Transmitted Infections, Chlamydia trachomatis, Neisseria gonorrhoeae, syphilis, and Trichomonas vaginalis: Methods and Results Used by the WHO to Generate 2005 Estimates","author":"World Health 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