CONICET | Buscador de Institutos y Recursos Humanos

Every day, more than one million people worldwide acquire a sexually transmitted infection (STI). This public health problem has a direct effect on womens reproductive and sexual health as STIs can cause irreversible damage to fertility and can have negative consequences associated with discrimination and social exclusion. Infection with one sexually transmitted pathogen predisposes to co-infection with others, suggesting the existence of shared pathways that serve as molecular links between these diseases. Galectins, a family of β-galactoside-binding proteins, have emerged as endogenous mediators that facilitate cell-surface binding, internalization and cell invasion of many sexually transmitted pathogens, including Chlamydia trachomatis, Neisseria gonorrhoeae, Trichomonas vaginalis, Candida albicans, HIV and herpes simplex virus. The ability of certain galectins to dimerize or form multimeric complexes confers the capacity to interact simultaneously with glycosylated ligands on both the pathogen and the cervico-vaginal tissue on these proteins. Galectins can act as a bridge by engaging glycans from the pathogen surface and glycosylated receptors from host cells, which is a mechanism that has been shown to be shared by several sexually transmitted pathogens. In the case of viruses and obligate intracellular bacteria, binding to the cell surface promotes pathogen internalization and cell invasion. Inflammatory responses that occur in cervico-vaginal tissue might trigger secretion of galectins, which in turn control the establishment, evolution and severity of STIs. Thus, galectin-targeted therapies could potentially prevent or decrease STIs caused by a diverse array of pathogenic microorganisms; furthermore, anti-galectin agents might reduce treatment costs of STIs and reach the most vulnerable populations.