• Parasites, Hosts and Diseases
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• v.54 no.1
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• pp.71-74
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• 2016

Trichomonas vaginalis is a flagellate protozoan parasite and commonly infected the lower genital tract in women and men. Iron is a known nutrient for growth of various pathogens, and also reported to be involved in establishment of trichomoniasis. However, the exact mechanism was not clarified. In this study, the author investigated whether the 120 kDa protein of T. vaginalis may be involved in pathogenicity of trichomonads. Antibodies against 120 kDa protein of T. vaginalis, which was identified as pyruvate:ferredoxin oxidoreductase (PFOR) by peptide analysis of MALDI-TOF-MS, were prepared in rabbits. Pretreatment of T. vaginalis with anti-120 kDa Ab decreased the proliferation and adherence to vaginal epithelial cells (MS74) of T. vaginalis. Subcutaneous tissue abscess in anti-120 kDa Ab-treated T. vaginalis-injected mice was smaller in size than that of untreated T. vaginalis-infected mice. Collectively, the 120 kDa protein expressed by iron may be involved in proliferation, adhesion to host cells, and abscess formation, thereby may influence on the pathogenicity of T. vaginalis.

• Parasites, Hosts and Diseases
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• v.51 no.4
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• pp.479-484
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• 2013

Neutrophils are the predominant inflammatory cells found in vaginal discharges of patients infected with Trichomonas vaginalis. In this study, we examined superoxide anion ($O^{\cdot}_{2^-}$) production by neutrophils activated by T. vaginalis. Human neutrophils produced superoxide anions when stimulated with either a lysate of T. vaginalis, its membrane component (MC), or excretory-secretory product (ESP). To assess the role of trichomonad protease in production of superoxide anions by neutrophils, T. vaginalis lysate, ESP, and MC were each pretreated with a protease inhibitor cocktail before incubation with neutrophils. Superoxide anion production was significantly decreased by this treatment. Trichomonad growth was inhibited by preincubation with supernatants of neutrophils incubated for 3 hr with T. vaginalis lysate. Furthermore, myeloperoxidase (MPO) production by neutrophils was stimulated by live trichomonads. These results indicate that the production of superoxide anions and MPO by neutrophils stimulated with T. vaginalis may be a part of defense mechanisms of neutrophils in trichomoniasis.

• Journal of Microbiology and Biotechnology
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• v.11 no.1
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• pp.124-130
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• 2001

The in vitro activities of 2,2'-dipyridyl, an iron-chelator, against clinical isolates of Trichomonas vaginalis, Candida albicans, and Gardnerella vaginalis was evaluated and compared with those of four other vaginal suppositories, ornidazole, clotrimazole, povidone-iodine, and $Cenacert^{\circledR}$ (Methylbezethonium Chloride mixed with 9-aminoacrydine undecylenate and hydrochloric acid N-myristyl-3-hydroxy butyl amine). The 2,2'-dipyridyl killed T. vaginalis and G. vaginalis at concentrations of $410\;{\mu}g/ml$ and $205\;{\mu}g/ml$, respectively, however, ths agent was less active against C. albicans (80% of which was inhiited at $410\;{\mu}g/ml$). The inhibition of these three pathogens by 2,2'-dipyridyl was similar to clotrimazole. In addition, the effect of 2,2'-dipyridyl on the ultrastructure of T. vaginalis, C. albicans, an G. vaginalis was examined. Transmission electron microscopy indicated that 2,2'-dipyridyl induced modifications of the cellular contents and cell envolope concumitant with the degradation of the three pathogens. These results suggest that 2,2'-dipyridyl has an inhibitory effect on C. albicans and G. vaginalis, as well as T. vaginalis.

• Parasites, Hosts and Diseases
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• v.54 no.2
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• pp.187-190
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• 2016

Trichomoniasis is the most common curable sexually-transmitted infection (STI) worldwide. There are few reports on the prevalence of Trichomonas vaginalis in Korea. The purpose of this study was to examine the prevalence of trichomoniasis by PCR in Guri city, Korea. All adult women who visited Hanyang University Guri Hospital for health screening within the National Health Care Service were invited to participate in the study, and 424 women were enrolled between March and June 2011. PCR was used to detect Trichomonas vaginalis using primers based on a repetitive sequence cloned from T. vaginalis (TV-E650). Fourteen women (3.3%) were found to have T. vaginalis. All were over 50, and they were significantly older on average than the 410 Trichomonas-negative women (mean ages 63.4 vs 55.3 years). It seems that T. vaginalis infection is not rare in women receiving health screening, especially among those over 50.

• Parasites, Hosts and Diseases
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• v.48 no.1
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• pp.1-7
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• 2010

Neutrophils play an important role in the human immune system for protection against such microorganisms as a protozoan parasite, Trichomonas vaginalis; however, the precise role of neutrophils in the pathogenesis of trichomoniasis is still unknown. Moreover, it is thought that trichomonal lysates and excretory-secretory products (ESP), as well as live T. vaginalis, could possibly interact with neutrophils in local tissues, including areas of inflammation induced by T. vaginalis in humans. The aim of this study was to investigate the influence of T. vaginalis lysate on the fate of neutrophils. We found that T. vaginalis lysate inhibits apoptosis of human neutrophils as revealed by Giemsa stain. Less altered mitochondrial membrane potential (MMP) and surface CD16 receptor expression also supported the idea that neutrophil apoptosis is delayed after T. vaginalis lysate stimulation. In contrast, ESP stimulated-neutrophils were similar in apoptotic features of untreated neutrophils. Maintained caspase-3 and myeloid cell leukemia-1 (Mcl-1) in neutrophils co-cultured with trichomonad lysate suggest that an intrinsic mitochondrial pathway of apoptosis was involved in T. vaginalis lysate-induced delayed neutrophil apoptosis; this phenomenon may contribute to local inflammation in trichomoniasis.

• Journal of Microbiology and Biotechnology
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• v.27 no.10
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• pp.1844-1854
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• 2017

Trichomonas vaginalis is a pathogen that triggers severe immune responses in hosts. T. vaginalis ${\alpha}$-actinin 2 ($Tv{\alpha}$-actinin 2) has been used to diagnose trichomoniasis. $Tv{\alpha}$-actinin 2 was dissected into three parts; the N-terminal, central, and C-terminal portions of the protein (#1, #2, and #3, respectively). Western blot of these $Tv{\alpha}$-actinin 2 proteins with pooled patients' sera indicated that #2 and #3, but not #1, reacted with those sera. Immunofluorescence assays of two different forms of T. vaginalis (trophozoites and amoeboid forms), using anti-$Tv{\alpha}$- actinin 2 antibodies, showed localization of $Tv{\alpha}$-actinin 2 close to the plasma membranes of the amoeboid form. Fractionation experiments indicated the presence of $Tv{\alpha}$-actinin 2 in cytoplasmic, membrane, and secreted proteins of T. vaginalis. Binding of fluorescence-labeled Trichomonas to vaginal epithelial cells and prostate cells was decreased in the antibody blocking experiment using anti-$Tv{\alpha}$-actinin 2 antibodies. Pretreatment of T. vaginalis with anti-$rTv{\alpha}$-actinin 2 antibodies also resulted in reduction in its cytotoxicity. Flow cytometry, ligand-binding immunoblotting assay, and observation by fluorescence microscopy were used to detect the binding of recombinant $Tv{\alpha}$-actinin 2 to human epithelial cell lines. Specifically, the truncated N-terminal portion of $Tv{\alpha}$-actinin 2, $Tv{\alpha}$-actinin 2 #1, was shown to bind directly to vaginal epithelial cells. These data suggest that ${\alpha}$-actinin 2 is one of the virulence factors responsible for the pathogenesis of T. vaginalis by serving as an adhesin to the host cells.

• BMB Reports
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• v.48 no.2
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• pp.103-108
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• 2015

Trichomoniasis caused by the parasitic protozoan Trichomonas vaginalis is the most common sexually transmitted disease in the world. Dendritic cells are antigen presenting cells that initiate immune responses by directing the activation and differentiation of naive T cells. In this study, we analyzed the effect of Trichomonas vaginalis-derived Secretory Products on the differentiation and function of dendritic cells. Differentiation of bone marrow-derived dendritic cells in the presence of T. vaginalis-derived Secretory Products resulted in inhibition of lipopolysaccharide-induced maturation of dendritic cells, down-regulation of IL-12, and up-regulation of IL-10. The protein components of T. vaginalis-derived Secretory Products were shown to be responsible for altered function of bone marrow-derived dendritic cells. Chromatin immunoprecipitation assay demonstrated that IL-12 expression was regulated at the chromatin level in T. vaginalis-derived Secretory Products-treated dendritic cells. Our results demonstrated that T. vaginalis- derived Secretory Products modulate the maturation and cytokine production of dendritic cells leading to immune tolerance.

• Journal of Microbiology and Biotechnology
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• v.16 no.12
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• pp.1984-1989
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• 2006

Deacetylated chitosan oligosaccharide (COS) had effective antiprotozoal activity against Trichomonas vaginalis (Minimal Inhibitory Concentration, MIC 0.25%), whereas 80% acetylated cas showed no antiprotozoal activity (MIC > 1 %). an the other hand, 80% acetylated cas showed growth stimulatory activity against the protozoa. When T. vaginalis was treated with 98% deacetylated COS at 0.25% concentration, the viability of the protozoa was rapidly decreased within 15 min, and the protozoa completely died within 40 min. Ultrastructural changes of trichomonads treated with COS included a loss of defined nuclear membrane and endoplasmic reticulum membranes, an increase in the number of free ribosome, vacuolation, and ultimately lysis of the cell membrane. These results indicate that deacetylated COS can be used as an antitrichomonal agent, although its lethal mechanism is not known.

• Parasites, Hosts and Diseases
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• v.52 no.6
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• pp.595-603
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• 2014

Trichomonas vaginalis secretes a number of proteases which are suspected to be the cause of pathogenesis; however, little is understood how they manipulate host cells. The mammalian target of rapamycin (mTOR) regulates cell growth, cell proliferation, cell motility, cell survival, protein synthesis, and transcription. We detected various types of metalloproteinases including GP63 protein from T. vaginalis trophozoites, and T. vaginalis GP63 metalloproteinase was confirmed by sequencing and western blot. When SiHa cells were stimulated with live T. vaginalis, T. vaginalis excretory-secretory products (ESP) or T. vaginalis lysate, live T. vaginalis and T. vaginalis ESP induced the mTOR cleavage in both time-and parasite load-dependent manner, but T. vaginalis lysate did not. Pretreatment of T. vaginalis with a metalloproteinase inhibitor, 1,10-phenanthroline, completely disappeared the mTOR cleavage in SiHa cells. Collectively, T. vaginalis metallopeptidase induces host cell mTOR cleavage, which may be related to survival of the parasite.

• Parasites, Hosts and Diseases
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• v.61 no.1
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• pp.2-14
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• 2023

Trichomonas vaginalis is a flagellated protozoan that causes trichomoniasis, a common nonviral sexually transmitted infection. T. vaginalis infection is asymptomatic in most infected men but can lead to chronic infection. The inflammatory response to chronic T. vaginalis infection may contribute to prostatic diseases, such as prostatitis and benign prostatic hyperplasia (BPH); however, studies on the relationship between T. vaginalis infection and prostate diseases are scarce. In this review, we discuss evidence from our studies on the involvement of T. vaginalis in the pathogenesis of prostate diseases, such as prostatitis and BPH. Studies of prostatitis have demonstrated that the attachment of T. vaginalis trophozoite to prostate epithelial cells (PECs) induces inflammatory cytokine production and inflammatory cell migration, leading to prostatitis. T. vaginalis also causes pathological changes, such as inflammatory cell infiltration, acinar changes, interstitial fibrosis, and mast cell infiltration, in prostate tissues of infected rats. Thus, T. vaginalis is considered an infectious agent that triggers prostatitis. Meanwhile, studies of prostatic hyperplasia revealed that mast cells activated by T. vaginalis-infected prostate cells secreted inflammatory mediators, such as β-hexosaminidase and tryptase, which promoted proliferation of prostate stromal cell (PSC). Moreover, interleukin-6 produced by proliferating PSCs induced the multiplication of BPH-1 epithelial cells as a result of stromal-epithelial interaction, suggesting that the proliferation of T. vaginalis-infected prostate cells can be induced through crosstalk with mast cells. These collective findings suggest that T. vaginalis contributes to the progression of prostatitis and prostatic hyperplasia by creating an inflammatory microenvironment involving PECs and PSCs.