Host immune consequences of asymptomatic Trichomonas vaginalis infection in pregnancy
Division of Maternal-Fetal Medicine, Magee-Womens Research Institute, Department of Obstetrics, Gynecology, and Reproductive Sciences, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA. American journal of obstetrics and gynecology
(Impact Factor: 4.7).
02/2007; 196(1):59.e1-5. DOI: 10.1016/j.ajog.2006.08.035
The purpose of this study was to define the impact of asymptomatic trichomoniasis on lower genital tract neutrophil activation in pregnancy.
In this nested cohort study, pelvic examination was performed on 65 asymptomatic pregnant women between 7 and 22 weeks' with vaginal pH > 4.4. Concentrations of cervical interleukin-8 and alpha-defensin were determined using enzyme-linked immunosorbent assay (ELISA). Trichomonas vaginalis was detected by culture.
Median concentrations of vaginal fluid neutrophil defensins and cervical interleukin-8 were significantly greater among women with asymptomatic trichomoniasis (median defensins 18,622 ng/mL, median IL-8 9244 pg/mL) than their uninfected counterparts (median defensins 5144 ng/mL, median IL-8 2044 pg/mL) (P < .001). All women with asymptomatic trichomoniasis had detectable defensin and interleukin-8 concentrations.
Asymptomatic trichomoniasis in pregnancy is accompanied by a state of neutrophil activation.
Available from: Theresa L Chang
- "Cationic peptides including defensins are required for anti-HIV activity of vaginal fluid from healthy women (Venkataraman et al., 2005). While it is well established that sexual transmitted infections (STIs) significantly increase the likelihood of HIV transmission (Chesson and Pinkerton, 2000; Cohen et al., 1997; Galvin and Cohen, 2004; Mabey, 2000; Plummer, 1998) and that levels of defensins including HNPs, HBDs and HD5 in genital fluid, are elevated in patients with STIs (Porter et al., 2005; Simhan et al., 2007; Valore et al., 2006; Wiesenfeld et al., 2002), the role of defensins in HIV transmission seems to be complex. "
Available from: Aprille Rapista
- "Defensins are antimicrobial peptides important to innate mucosal immunity [6-9]. Indeed, the levels of defensins in genital fluid are frequently elevated in individuals with STIs [10-13], suggesting a potential role of defensins in modulating HIV transmission. Recently, antimicrobial peptides including human neutrophil defensins 1-3 (HNPs 1-3) and LL-37 have been found to be increased in cervicovaginal secretions from women with STIs and are independently associated with increased HIV acquisition . "
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ABSTRACT: Concurrent sexually transmitted infections (STIs) increase the likelihood of HIV transmission. The levels of defensins are frequently elevated in genital fluids from individuals with STIs. We have previously shown that human defensins 5 and 6 (HD5 and HD6) promote HIV entry and contribute to Neisseria gonorrhoeae-mediated enhancement of HIV infectivity in vitro. In this study, we dissect the molecular mechanism of the HIV enhancing effect of defensins.
HD5 and HD6 primarily acted on the virion to promote HIV infection. Both HD5 and HD6 antagonized the anti-HIV activities of inhibitors of HIV entry (TAK 779) and fusion (T-20) when the inhibitors were present only during viral attachment; however, when these inhibitors were added back during viral infection they overrode the HIV enhancing effect of defensins. HD5 and HD6 enhanced HIV infectivity by promoting HIV attachment to target cells. Studies using fluorescent HIV containing Vpr-GFP indicated that these defensins enhanced HIV attachment by concentrating virus particles on the target cells. HD5 and HD6 blocked anti-HIV activities of soluble glycosaminoglycans including heparin, chondroitin sulfate, and dextran sulfate. However, heparin, at a high concentration, diminished the HIV enhancing effect of HD5, but not HD6. Additionally, the degree of the HIV enhancing effect of HD5, but not HD6, was increased in heparinase-treated cells. These results suggest that HD5 and haparin/heparan sulfate compete for binding to HIV.
HD5 and HD6 increased HIV infectivity by concentrating virus on the target cells. These defensins may have a negative effect on the efficacy of microbicides, especially in the setting of STIs.
Available from: Raina Fichorova
- "At the same time in symptomatic women, antiinflammatory mediators such as the soluble leukocyte protease inhibitor (SLPI) were lower (possibly due to digestion by trichomonas cysteine proteases) and reactive nitrogen intermediates were higher (Al-Mohammed and Hussein, 2006; Draper et al., 1998). The presence of increased C-reactive protein in the sera of T. vaginalis-infected pregnant women suggests that the impact of the immunoinflammatory reaction to the parasite exceeds the boundaries of the reproductive tract mucosa (Simhan et al., 2007). Mechanisms of pregnancy complications linked to T. vaginalis remain elusive. "
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ABSTRACT: Trichomonas vaginalis is the most common non-viral sexually transmitted pathogen. The infection is prevalent in reproductive age women and is associated with vaginitis, endometritis, adnexitis, pyosalpinx, infertility, preterm birth, low birth weight, bacterial vaginosis, and increased risk of cervical cancer, HPV, and HIV infection. In men, its complications include urethritis, prostatitis, epididymitis, and infertility through inflammatory damage or interference with the sperm function. The infection is often asymptomatic and recurrent despite the presence of specific antibodies, suggesting the importance of the innate immune defense. T. vaginalis adhesion proteins, cysteine proteases, and the major parasite lipophosphoglycan (LPG) play distinct roles in the pathogenesis and evasion of host immunity. LPG plays a key role in the parasite adherence and signaling to human vaginal and cervical epithelial cells, which is at least in part mediated by galectins. The epithelial cells respond to T. vaginalis infection and purified LPG by selective upregulation of proinflammatory mediators. At the same time, T. vaginalis triggers an immunosuppressive response in monocytes, macrophages, and dendritic cells. The molecular mechanisms underlying reproductive complications and epidemiologic risks associated with T. vaginalis infection remain to be elucidated.
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