Okumura, C. Y., Baum, L. G. & Johnson, P. J. Galectin-1 on cervical epithelial cells is a receptor for the sexually transmitted human parasite Trichomonas vaginalis. Cell. Microbiol. 1, 2078-2090

Department of Microbiology, Immunology, and Molecular Genetics, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA 90095, USA.
Cellular Microbiology (Impact Factor: 4.92). 10/2008; 10(10):2078-90. DOI: 10.1111/j.1462-5822.2008.01190.x
Source: PubMed


The extracellular protozoan parasite Trichomonas vaginalis causes the most prevalent non-viral sexually transmitted human infection, yet the pathogenesis of infection is poorly understood, and host cell receptors have not been described. The surface of T. vaginalis is covered with a glycoconjugate called lipophosphoglycan (LPG), which plays a role in the adherence and cytotoxicity of parasites to human cells. T. vaginalis LPG contains high amounts of galactose, making this polysaccharide a candidate for recognition by the galactose-binding galectin family of lectins. Here we show that galectin-1 (gal-1) is expressed by human cervical epithelial cells and binds T. vaginalis LPG. Gal-1 binds to parasites in a carbohydrate-dependent manner that is inhibited in the presence of T. vaginalis LPG. Addition of purified gal-1 to cervical epithelial cells also enhances parasite binding, while a decrease in gal-1 expression by small interfering RNA (siRNA) transfection decreases parasite binding. In contrast, the related galectin-7 (gal-7) does not bind T. vaginalis in a carbohydrate-dependent manner, and is unable to mediate attachment of parasites to host cells. Our data are consistent with the presence of multiple host cell receptors for T. vaginalis of which gal-1 is the first to be identified and highlight the importance of glycoconjugates in host-pathogen interactions.

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Available from: Cheryl Y M Okumura, Jan 05, 2015
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    • "Trichomonas vaginalis disrupts urogenital epithelial layers facilitating HIV-1 passage to underlying layers and activates local immune cells leading to increased viral replication[25]. Host cervical cells express a multitude of receptors for the binding of Trichomonas[26], and cytolysis of 80–90% of cervical cells is caused by Trichomonas contact[27]. Cysteine proteases (thiol proteases) that play a vital role in cytoadherence of parasites to host cells[28,29]are readily detected in vaginal washes of infected women[30], causing apoptosis of vaginal cells[31]. "
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    • "Interestingly, we found that most of the TvTSPs analysed were up-regulated upon contact with VECs, suggesting a role for these proteins in host : parasite interaction. Since in vitro attachment of the parasites is mostly completed within ∼ 20 min of exposure to the VECs (Okumura et al., 2008), the pattern of up-regulation suggests TvTSPs plays a role in events occurring downstream of adherence. It is important to note that while most of the TvTSP genes we found were up regulated upon exposure of B7RC2 strain to host cells, these genes were not reported in the up regulated group in the Gould et al. analysis (Gould et al., 2013). "
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