Open Access
Galectin‐1 on cervical epithelial cells is a receptor for the sexually transmitted human parasite Trichomonas vaginalis
Author(s) -
Okumura Cheryl Y. M.,
Baum Linda G.,
Johnson Patricia J.
Publication year - 2008
Publication title -
cellular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.542
H-Index - 138
eISSN - 1462-5822
pISSN - 1462-5814
DOI - 10.1111/j.1462-5822.2008.01190.x
Subject(s) - trichomonas vaginalis , biology , glycoconjugate , lipophosphoglycan , microbiology and biotechnology , galectin , transfection , receptor , galectin 3 , virology , cell culture , immunology , biochemistry , genetics , leishmaniasis , visceral leishmaniasis , leishmania donovani
Summary 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.