Fichorova1, R., Trifonova1, R., Gilbert2, R., Costello3, C., Hayes4, G., Lucas4, J., and Singh4, B. 1Laboratory of Genital Tract Biology, Department of Obstetrics, Gynecology and Reproductive Biology, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA; 2Department of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY; 3Mass Spectrometry Resource, Boston University School of Medicine, Boston, MA; and 4Department of Biochemistry and Molecular Biology, SUNY Upstate Medical University, Syracuse, NY.

This study by researchers at Brigham and Women’s Hospital/Harvard Medical School, Cornell University, Boston University School of Medicine, and SUNY Upstate Medical University demonstrated that MatTek’s EpiVaginal human cervico-vaginal tissue equivalent can be used to study in vitro the molecular pathways important in initiating host inflammatory and immune responses to Trichomonas vaginalis. Trichomonas vaginalis is one of the most common non-viral sexually transmitted human infections and, worldwide, has been linked to increased incidence of human immunodeficiency virus type 1 (HIV-1) transmission, preterm delivery, low birth weight, cervical cancer, and vaginitis. The molecular pathways that are important in initiating host inflammatory and immune responses to T. vaginalis are poorly understood. In this paper, researchers report on interactions of human cervicovaginal epithelial cells (MatTek’s EpiVaginal human tissue equivalent) with the most abundant cell surface glycoconjugate of the parasite, the T. vaginalis lipophosphoglycan (LPG). Purified LPG mediated the adhesion of parasites to human vaginal epithelial tissues (EpiVaginal) in a dose-dependent manner. Furthermore, T. vaginalis LPG (but not LPG from Tritrichomonas foetus, the causative agent of bovine trichomoniasis) induced a selective upregulation of chemotactic cytokines by human endocervical, ectocervical, and vaginal epithelial cells, which do not express Toll-like receptor 4/MD2. The T. vaginalis LPG triggered interleukin 8 (IL-8), which promotes the adhesion and transmigration of neutrophils across the endothelium, and macrophage inflammatory protein 3á, which is a chemoattractant for immune cells and is essential for dendritic cell maturation. These effects were dose dependent and sustained in the absence of cytotoxicity and IL-1â release and utilized, at least in part, a signaling pathway independent from the Toll-like/IL-1 receptor adaptor protein MyD88.


EpiVaginal, Gas-liquid chromatography-mass spectrometry, Glycosylated phosphatidylinositol (GPI), HIV-1, Inflammation, Inflammatory, Inflammatory response, Interleukin 1b, Interleukin 6 (IL-6), Interleukin 8 (IL-8), Lipophosphoglycan (LPG), Luciferase assay, MYD88, P-NF-KB, Sexually transmitted infections, Toll-Like Receptor 4/MD2, Trichomonas vaginalis, Tritrichomonas foetus, Tumor necrosis factor alpha (TNF-a), VEC-100, Vaginitis, p-NF-KB

Materials Tested

Alpha’-mannosidase, Beta-Galactosidase, Beta-N-acetylhexosaminidase , Beta-mannosidase, Cysteine-methionine , Diamond’s Trypticase-yeast extract medium, Ectocervical epithelial cells, EpiVaginal (VEC-100), Gas-liquid chromatography-mass spectrometry, High-performance anion exchange-pulse amperometirc detector, Human cervicovagianl epithelial cells, Lactate dehydrogenase (LDH), MTT assay, Mannose (Man), Phosphate Buffered Solution (PBS), UR1, endo-beta-galactosidase

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