Infinity war: Trichomonas vaginalis and interactions with host immune response
Authors:Giulia Bongiorni Galego1 and Tiana Tasca1
doi: 10.15698/mic2023.05.796
Volume 10, pp. 103 to 116, published 30/03/2023.
1 Grupo de Pesquisa em Tricomonas, Faculdade de Farmácia e Centro de Biotecnologia, Universidade Federal do Rio Grande do Sul, Avenida Ipiranga, 2752, Porto Alegre, 90610-000, Rio Grande do Sul, Brazil.
Keywords:
trichomoniasis, Trichomonas vaginalis, immune response, inflammation.
Corresponding Author(s):
Conflict of interest statement:
Authors declare no conflict of interest.
Please cite this article as:
Giulia Bongiorni Galego and Tiana Tasca (2023). Infinity war: Trichomonas vaginalis and interactions with host immune response. Microbial Cell 10(5): 103-116. doi: 10.15698/mic2023.05.796
© 2023 Bongiorni Galego and Tasca. This is an open-access article released under the terms of the Creative Commons Attribution (CC BY) license, which allows the unrestricted use, distribution, and reproduction in any medium, provided the original author and source are acknowledged.
Abstract:
Trichomonas vaginalis is the pathological agent of human trichomoniasis. 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, cervical and prostate cancer, and adverse outcomes during pregnancy, increasing our understanding of the pathogen’s interaction with the host immune response is essential. Production of cytokines and cells of innate immunity: Neutrophils and macrophages are the main cells involved 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 inflammatory environment that may lead to preterm birth. Endosymbiosis: 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 serum samples of rodents infected with isolates from symptomatic patients as well as patients with symptoms. However, antibody production 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 targets 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.