Proliferation of Prostate Stromal Cell Induced by Benign Prostatic Hyperplasia Epithelial Cell Stimulated With<i>Trichomonas vaginalis</i>via Crosstalk With Mast Cell

Kim, Jung-Hyun; Kim, Sang-Su; Han, Ik-Hwan; Sim, Seobo; Ahn, Myoung-Hee; Ryu, Jae‐Sook

doi:10.1002/pros.23227

Cited by 35 publications

(74 citation statements)

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“…We previously reported that CCL2 produced by T. vaginalis infection in vaginal epithelial cells induced the migration of mast cells . Moreover, our in vitro study showed that mast cells were involved in the proliferation of stromal cells caused by inflammation of prostate epithelial cells stimulated with T. vaginalis . In the present in vivo model, we noted increased numbers of mast cells and degranulated mast cells in the prostate tissues infected with T. vaginalis (Figures and ).…”

Section: Discussionsupporting

confidence: 69%

Experimental rat prostatitis caused by Trichomonas vaginalis infection

et al. 2018

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Background Trichomonas vaginalis (T. vaginalis) is the most common sexually transmitted parasite. It has been detected in prostatic tissue of patients with prostatitis and reported to be associated with chronic prostatitis and benign prostatic hyperplasia as well as prostate cancer. Recently, experimental rodent models of prostatitis induced by pathogen infection have been developed. However, there have so far been no reports of prostatitis caused by T. vaginalis infection in animals. Here, we investigated whether infection with T. vaginalis via the rat urethra could cause prostatitis. Methods T. vaginalis was injected into prostate through urethra of rat (Wistar rats), and the rats were killed 1, 2, or 4 weeks later. The presence of T. vaginalis trophozoites in the rat prostates was examined by immunohistochemistry, and pathological changes of the prostate were observed by hematoxylin‐eosin staining and evaluated by grading from 0 to 5 for inflammatory cell infiltration, acinar changes, and interstitial fibrosis. Infiltrated mast cells were observed by toluidine blue staining of rat prostate tissue. Chemokine C‐C motif ligand 2 (CCL2) levels of the rat prostates were measured by ELISA. Results T. vaginalis trophozoites were observed in acini in the prostates of the injected rats. The prostate tissues had higher pathological scores, and 83% (5/6) and 100% (6/6) of the ventral and dorsolateral lobes (n = 6), respectively, were inflamed. Infiltration and degranulation of mast cells were observed at higher rates in prostate sections of the T. vaginalis‐infected rats. Also, prostate tissues of the injected rats had increased CCL2 levels. Conclusions Injection of T. vaginalis in rats caused prostatitis as revealed by pathologic changes, mast cell infiltration and increased CCL2 production. Therefore, this study provides the first evidence that T. vaginalis infection in rats causes prostatitis.

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Section: Discussionsupporting

confidence: 69%

Experimental rat prostatitis caused by Trichomonas vaginalis infection

et al. 2018

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“…There are recent reports of a high infection rate (21.2%) of Tv in patients with chronic recurrent prostatitis and urethritis in Korea, and a high detection rate (34%) of Tv in benign prostatic hyperplasia (BPH) tissue . We showed previously that Tv stimulation of prostatic epithelial and stroma cells in vitro induced an inflammatory response through the production of chronic inflammatory cytokines, such as interleukin (IL)‐1β, IL‐6, and C‐X‐C motif ligand 8 (CXCL8), which there are high levels in the seminal fluid of patients with chronic prostatitis/chronic pelvic pain syndrome (CP/CCPS) …”

Section: Introductionmentioning

confidence: 99%

“…4,5 We showed previously that Tv stimulation of prostatic epithelial and stroma cells in vitro induced an inflammatory response through the production of chronic inflammatory cytokines, such as interleukin (IL)-1β, IL-6, and C-X-C motif ligand 8 (CXCL8), which there are high levels in the seminal fluid of patients with chronic prostatitis/chronic pelvic pain syndrome (CP/CCPS). [6][7][8][9][10] Inflammation has been implicated as a carcinogen in a number of human cancers, and in a number of organs, 11,12 and a variety of epidemiological and histopathological findings have suggested that prostate cancer (PCa) risk is correlated with inflammation. 13 The pathogenesis of PCa involves multiple genes as well as environmental factors, such as diet and inflammation.…”

Section: Introductionmentioning

confidence: 99%

Inflammatory mediators of prostate epithelial cells stimulated with Trichomonas vaginalis promote proliferative and invasive properties of prostate cancer cells

et al. 2019

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Background Trichomonas vaginalis (Tv) is the most common sexually transmitted parasite. It is detected in prostatic tissue of benign prostatic hyperplasia, prostatitis, and prostate cancer (PCa) and has been suggested to cause chronic prostatitis. Moreover, up to 20% of all cancers worldwide are associated with chronic inflammation. Here, we investigated whether inflammatory mediators produced by normal human prostate epithelial cells (RWPE‐1) stimulated with Tv could promote growth and invasiveness of PCa cells. Methods Conditioned medium of RWPE‐1 cells was prepared by stimulating them with Tv (trichomonad‐conditioned medium [TCM]) and without Tv (conditioned medium [CM]). Promotion of PCa cells (PC3, DU145, and LNCaP) was assessed by wound healing, proliferation, and invasion assays. Results We observed that the production of interleukin (IL)‐1β, IL‐6, CCL2, CXCL8, prostaglandin‐E2 (PGE2), and COX2 by RWPE‐1 cells was increased by stimulating them with Tv. When PCa cells were incubated with TCM, their proliferation, invasion, and migration increased. Moreover, they showed increased epithelial‐mesenchymal transition (EMT)‐related markers by a reduction in epithelial markers and an increase in mesenchymal markers. In vivo, xenograft tumor tissues injected with TCM also showed increased expression of cyclin D1 and proliferating cell nuclear antigen, as well as induction of EMT. Receptors and signal molecules of PCa cells increased in response to exposure to TCM, and blocking receptors (CXCR1, CXCR2, C‐C chemokine receptor 2, glycoprotein 130, EP2, and EP4) reduced the proliferation of PCa cells with decreased production of cytokines (CCL2, IL‐6, and CXCL8) and PGE2, and expression of NF‐κB and Snail1. CONCLUSIONS Our results suggest that Tv infection may be one of the factors creating the supportive microenvironment to promote proliferation and invasiveness of PCa cells.

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“…Possible mechanisms by which it may contribute to these conditions include: (a) adherence to and lysis of prostate epithelial cells; (b) induction of intra‐prostatic inflammation and cytokine production; (c) inhibition of prostate epithelial cell apoptosis; and (d) upregulation of proto‐oncogenes . More recently, T. vaginalis has also been observed to increase prostate cell line proliferation and invasiveness, has been detected in prostate tissue from men with BPH, and has been found to be associated with the presence of BPH, as well as later prostate cancer risk and aggressiveness in some, but not all, sero‐epidemiologic studies.…”

Section: Introductionmentioning

confidence: 99%

“…These suggestive findings may be relevant for prostate condition development because higher early-to mid-life PSA concentrations have been found to predict greater prostate cancer risk later in life. 1,2 More recently, T. vaginalis has also been observed to increase prostate cell line proliferation and invasiveness, 3,4 has been detected in prostate tissue from men with BPH, 2,5 and has been found to be associated with the presence of BPH, 6 as well as later prostate cancer risk and aggressiveness in some, 7,8 but not all, [9][10][11][12][13][14] sero-epidemiologic studies.…”

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confidence: 99%

Trichomonas vaginalis infection and prostate‐specific antigen concentration: Insights into prostate involvement and prostate disease risk

et al. 2019

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Background: The protist Trichomonas vaginalis causes a common, sexually transmitted infection and has been proposed to contribute to the development of chronic prostate conditions, including benign prostatic hyperplasia and prostate cancer. However, few studies have investigated the extent to which it involves the prostate in the current antimicrobial era. We addressed this question by investigating the relation between T. vaginalis antibody serostatus and serum prostate‐specific antigen (PSA) concentration, a marker of prostate infection, inflammation, and/or cell damage, in young, male, US military members. Methods: We measured T. vaginalis serum IgG antibodies and serum total PSA concentration in a random sample of 732 young, male US active duty military members. Associations between T. vaginalis serostatus and PSA were investigated by linear regression. Results: Of the 732 participants, 341 (46.6%) had a low T. vaginalis seropositive score and 198 (27.0%) had a high score, with the remainder seronegative. No significant differences were observed in the distribution of PSA by T. vaginalis serostatus. However, slightly greater, nonsignificant differences were observed when men with high T. vaginalis seropositive scores were compared with seronegative men, and when higher PSA concentrations were examined (≥0.70 ng/mL). Specifically, 42.5% of men with high seropositive scores had a PSA concentration greater than or equal to 0.70 ng/mL compared with 33.2% of seronegative men (adjusted P = .125). Conclusions: Overall, our findings do not provide strong support for prostate involvement during T. vaginalis infection, although our suggestive positive findings for higher PSA concentrations do not rule out this possibility entirely. These suggestive findings may be relevant for prostate condition development because higher early‐ to mid‐life PSA concentrations have been found to predict greater prostate cancer risk later in life.

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Proliferation of Prostate Stromal Cell Induced by Benign Prostatic Hyperplasia Epithelial Cell Stimulated WithTrichomonas vaginalisvia Crosstalk With Mast Cell

Cited by 35 publications

References 50 publications

Experimental rat prostatitis caused by Trichomonas vaginalis infection

Experimental rat prostatitis caused by Trichomonas vaginalis infection

Inflammatory mediators of prostate epithelial cells stimulated with Trichomonas vaginalis promote proliferative and invasive properties of prostate cancer cells

Trichomonas vaginalis infection and prostate‐specific antigen concentration: Insights into prostate involvement and prostate disease risk

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