Infinity war : Trichomonas vaginalis and interactions with host immune response

Detalhes bibliográficos
Autor(a) principal: Galego, Giulia Bongiorni
Data de Publicação: 2023
Outros Autores: Tasca, Tiana
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Institucional da UFRGS
Texto Completo: http://hdl.handle.net/10183/259969
Resumo: 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 out-comes during pregnancy, increasing our understanding of the patho-gen’s interaction with the host immune response is essential. Produc-tion of cytokines and cells of innate immunity: Neutrophils and mac-rophages 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 re-sponse 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 sig-naling: NTPD-ases and ecto-5’-nucleotidase helps in parasite survival by modulating the nucleotides levels in the microenvironment. Anti-bodies: IgG was detected in serum samples of rodents infected with isolates from symptomatic patients as well as patients with symp-toms. However, antibody production does not protect against a rein-fection. 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 develop-ment. 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 trichomoni-asis.
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spelling Galego, Giulia BongiorniTasca, Tiana2023-07-04T03:52:42Z20232311-2638http://hdl.handle.net/10183/259969001168389Trichomonas 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 out-comes during pregnancy, increasing our understanding of the patho-gen’s interaction with the host immune response is essential. Produc-tion of cytokines and cells of innate immunity: Neutrophils and mac-rophages 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 re-sponse 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 sig-naling: NTPD-ases and ecto-5’-nucleotidase helps in parasite survival by modulating the nucleotides levels in the microenvironment. Anti-bodies: IgG was detected in serum samples of rodents infected with isolates from symptomatic patients as well as patients with symp-toms. However, antibody production does not protect against a rein-fection. 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 develop-ment. 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 trichomoni-asis.application/pdfengMicrobial cell. [Graz]. Vol. 10, n. 5 (2023), p. 103-116TricomoníaseTrichomonas vaginalisImunidadeInflamaçãoTrichomoniasisImmune responseInflammationInfinity war : Trichomonas vaginalis and interactions with host immune responseEstrangeiroinfo:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UFRGSinstname:Universidade Federal do Rio Grande do Sul (UFRGS)instacron:UFRGSTEXT001168389.pdf.txt001168389.pdf.txtExtracted Texttext/plain80555http://www.lume.ufrgs.br/bitstream/10183/259969/2/001168389.pdf.txt311e2bf6e250a0cfee3ea6d58feccab0MD52ORIGINAL001168389.pdfTexto completo (inglês)application/pdf801047http://www.lume.ufrgs.br/bitstream/10183/259969/1/001168389.pdf82c164cfa8809bd5e0190870fdd66ea3MD5110183/2599692023-07-05 03:49:51.556895oai:www.lume.ufrgs.br:10183/259969Repositório de PublicaçõesPUBhttps://lume.ufrgs.br/oai/requestopendoar:2023-07-05T06:49:51Repositório Institucional da UFRGS - Universidade Federal do Rio Grande do Sul (UFRGS)false
dc.title.pt_BR.fl_str_mv Infinity war : Trichomonas vaginalis and interactions with host immune response
title Infinity war : Trichomonas vaginalis and interactions with host immune response
spellingShingle Infinity war : Trichomonas vaginalis and interactions with host immune response
Galego, Giulia Bongiorni
Tricomoníase
Trichomonas vaginalis
Imunidade
Inflamação
Trichomoniasis
Immune response
Inflammation
title_short Infinity war : Trichomonas vaginalis and interactions with host immune response
title_full Infinity war : Trichomonas vaginalis and interactions with host immune response
title_fullStr Infinity war : Trichomonas vaginalis and interactions with host immune response
title_full_unstemmed Infinity war : Trichomonas vaginalis and interactions with host immune response
title_sort Infinity war : Trichomonas vaginalis and interactions with host immune response
author Galego, Giulia Bongiorni
author_facet Galego, Giulia Bongiorni
Tasca, Tiana
author_role author
author2 Tasca, Tiana
author2_role author
dc.contributor.author.fl_str_mv Galego, Giulia Bongiorni
Tasca, Tiana
dc.subject.por.fl_str_mv Tricomoníase
Trichomonas vaginalis
Imunidade
Inflamação
topic Tricomoníase
Trichomonas vaginalis
Imunidade
Inflamação
Trichomoniasis
Immune response
Inflammation
dc.subject.eng.fl_str_mv Trichomoniasis
Immune response
Inflammation
description 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 out-comes during pregnancy, increasing our understanding of the patho-gen’s interaction with the host immune response is essential. Produc-tion of cytokines and cells of innate immunity: Neutrophils and mac-rophages 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 re-sponse 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 sig-naling: NTPD-ases and ecto-5’-nucleotidase helps in parasite survival by modulating the nucleotides levels in the microenvironment. Anti-bodies: IgG was detected in serum samples of rodents infected with isolates from symptomatic patients as well as patients with symp-toms. However, antibody production does not protect against a rein-fection. 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 develop-ment. 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 trichomoni-asis.
publishDate 2023
dc.date.accessioned.fl_str_mv 2023-07-04T03:52:42Z
dc.date.issued.fl_str_mv 2023
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dc.identifier.issn.pt_BR.fl_str_mv 2311-2638
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dc.language.iso.fl_str_mv eng
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dc.relation.ispartof.pt_BR.fl_str_mv Microbial cell. [Graz]. Vol. 10, n. 5 (2023), p. 103-116
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