The Role of Purinergic Signaling in Trichomonas vaginalis Infection

Abstract

Trichomoniasis, one of the most common non-viral sexually transmitted infections worldwide, is caused by the parasite Trichomonas vaginalis. The pathogen colonizes the human urogenital tract, and the infection is associated with complications such as adverse pregnancy outcomes, cervical cancer, and an increase in HIV transmission. The mechanisms of pathogenicity are multifactorial, and controlling immune responses is essential for infection maintenance. Extracellular purine nucleotides are released by cells in physiological and pathological conditions, and they are hydrolyzed by enzymes called ecto-nucleotidases. The cellular effects of nucleotides and nucleosides occur via binding to purinoceptors, or through the uptake by nucleoside transporters. Altogether, enzymes, receptors and transporters constitute the purinergic signaling, a cellular network that regulates several effects in practically all systems including mammals, helminths, protozoa, bacteria, and fungi. In this context, this review updates the data on purinergic signaling involved in T. vaginalis biology and interaction with host cells, focusing on the characterization of ecto-nucleotidases and on purine salvage pathways. The implications of the final products, the nucleosides adenosine and guanosine, for human neutrophil response and vaginal epithelial cell damage reveal the purinergic signaling as a potential new mechanism for alternative drug targets.

Keywords: Adenosine; Immune response; Neutrophils; Purinergic signaling; Trichomonas vaginalis; Vaginal epithelial cells.