Infinity war: Trichomonas vaginalis and interactions with host immune response

Abstract

Trichomonas vaginalis is the pathological agent of human trichomonia-sis. The incidence is 156 million cases worldwide. Due to the increasing resistance of isolates to approved drugs and clinical complications that include increased risk in the acquisition and transmission of HIV, cervi-cal and prostate cancer, and adverse outcomes during pregnancy, in-creasing our understanding of the pathogen’s interaction with the host immune response is essential. Production of cytokines and cells of in-nate immunity: Neutrophils and macrophages are the main cells in-volved in the fight against the parasite, while IL-8, IL-6 and TNF-α are the most produced cytokines in response to this infection. Clinical complications: T. vaginalis increases the acquisition of HIV, stimulates the invasiveness and growth of prostate cells, and generates an in-flammatory environment that may lead to preterm birth. Endosymbi-osis: Mycoplasma hominis increased cytotoxicity, growth, and survival rate of the parasite. Purinergic signaling: NTPD-ases and ecto-5’-nucleotidase helps in parasite survival by modulating the nucleotides levels in the microenvironment. Antibodies: IgG was detected in se-rum samples of rodents infected with isolates from symptomatic pa-tients as well as patients with symptoms. However, antibody produc-tion does not protect against a reinfection. Vaccine candidate targets: The transient receptor potential- like channel of T. vaginalis (TvTRPV), cysteine peptidase, and α-actinin are currently cited as candidate tar-gets for vaccine development. In this context, the understanding of mechanisms involved in the host-T. vaginalis interaction that elicit the immune response may contribute to the development of new targets to combat trichomoniasis.

Keywords

• trichomoniasis
• trichomonas vaginalis
• immune response
• inflammation