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Infection and Immunity, October 2006, p. 5773-5779, Vol. 74, No. 10
0019-9567/06/$08.00+0     doi:10.1128/IAI.00631-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Trichomonas vaginalis Lipophosphoglycan Triggers a Selective Upregulation of Cytokines by Human Female Reproductive Tract Epithelial Cells

Raina N. Fichorova,1* Radiana T. Trifonova,1 Robert O. Gilbert,2 Catherine E. Costello,3 Gary R. Hayes,4 John J. Lucas,4 and Bibhuti N. Singh4

Laboratory of Genital Tract Biology, Department of Obstetrics, Gynecology and Reproductive Biology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts,1 Department of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, New York,2 Mass Spectrometry Resource, Boston University School of Medicine, Boston, Massachusetts,3 Department of Biochemistry and Molecular Biology, SUNY Upstate Medical University, Syracuse, New York4

Received 19 April 2006/ Returned for modification 13 June 2006/ Accepted 23 July 2006

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 to T. vaginalis are poorly understood. Here we report interactions of human cervicovaginal epithelial cells 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 cells 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 3{alpha}, 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-1ß release and utilized, at least in part, a signaling pathway independent from the Toll-like/IL-1 receptor adaptor protein MyD88.

* Corresponding author. Mailing address: Laboratory of Genital Tract Biology, Department of Obstetrics, Gynecology and Reproductive Biology, Harvard Medical School, Brigham and Women's Hospital, 221 Longwood Avenue, RF468, Boston, MA 02115. Phone: (617) 278-0625. Fax: (617) 713-3018. E-mail: rfichorova{at}partners.org.

Editor: J. F. Urban, Jr.

Infection and Immunity, October 2006, p. 5773-5779, Vol. 74, No. 10
0019-9567/06/$08.00+0     doi:10.1128/IAI.00631-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Trifonova, R. T., Doncel, G. F., Fichorova, R. N. (2009). Polyanionic Microbicides Modify Toll-Like Receptor-Mediated Cervicovaginal Immune Responses. Antimicrob. Agents Chemother. 53: 1490-1500 [Abstract] [Full Text]  
  • Grabinska, K. A., Ghosh, S. K., Guan, Z., Cui, J., Raetz, C. R. H., Robbins, P. W., Samuelson, J. (2008). Dolichyl-Phosphate-Glucose Is Used To Make O-Glycans on Glycoproteins of Trichomonas vaginalis. Eukaryot Cell 7: 1344-1351 [Abstract] [Full Text]  


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