Open AccessTrichomonas vaginalisLipophosphoglycan Triggers a Selective Upregulation of Cytokines by Human Female Reproductive Tract Epithelial Cells
Author(s) -
Rai. Fichorova,
Radiana Trifonova,
R.O. Gilbert,
Catherine E. Costello,
Gary R. Hayes,
John J. Lucas,
Bibhuti N. Singh
Publication year - 2006
Publication title -
infection and immunity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.508
H-Index - 220
eISSN - 1070-6313
pISSN - 0019-9567
DOI - 10.1128/iai.00631-06
Subject(s) - biology , lipophosphoglycan , trichomonas vaginalis , trichomoniasis , immunology , immune system , ccl20 , downregulation and upregulation , cytokine , microbiology and biotechnology , chemokine , medicine , chemokine receptor , biochemistry , pathology , leishmaniasis , visceral leishmaniasis , leishmania donovani , gene
Trichomonas vaginalis is one of the most common nonviral sexually transmitted human infections and, worldwide, has been linked to increased incidence of human immunodeficiency virus type 1 transmission, preterm delivery, low birth weight, cervical cancer, and vaginitis. The molecular pathways that are important in initiating host inflammatory and immune responses toT. vaginalis are poorly understood. Here we report interactions of human cervicovaginal epithelial cells with the most abundant cell surface glycoconjugate of the parasite, theT. vaginalis lipophosphoglycan (LPG). Purified LPG mediated the adhesion of parasites to human vaginal epithelial cells in a dose-dependent manner. Furthermore,T. vaginalis LPG (but not LPG fromTritrichomonas 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. TheT. vaginalis LPG triggered interleukin 8 (IL-8), which promotes the adhesion and transmigration of neutrophils across the endothelium, and macrophage inflammatory protein 3α, 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-1β release and utilized, at least in part, a signaling pathway independent from the Toll-like/IL-1 receptor adaptor protein MyD88.