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Changes of the Intestinal Microbiome–Host Homeostasis in HIV-Infected Individuals – A Focus on the Bacterial Gut Microbiome

Human immunodeficiency virus (HIV) infections cause severe CD4+ T cell depletion leading to chronic inflammation and immune activation, impaired barrier function, and microbial translocation. Even under effective antiretroviral therapy, these processes persist, leading to gut microbiome dysbiosis an...

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Autores principales: Ribeiro, Ana Beatriz Dein Terra Mota, Heimesaat, Markus M., Bereswill, Stefan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Akadémiai Kiadó 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5632743/
https://www.ncbi.nlm.nih.gov/pubmed/29034105
http://dx.doi.org/10.1556/1886.2017.00016
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author Ribeiro, Ana Beatriz Dein Terra Mota
Heimesaat, Markus M.
Bereswill, Stefan
author_facet Ribeiro, Ana Beatriz Dein Terra Mota
Heimesaat, Markus M.
Bereswill, Stefan
author_sort Ribeiro, Ana Beatriz Dein Terra Mota
collection PubMed
description Human immunodeficiency virus (HIV) infections cause severe CD4+ T cell depletion leading to chronic inflammation and immune activation, impaired barrier function, and microbial translocation. Even under effective antiretroviral therapy, these processes persist, leading to gut microbiome dysbiosis and disturbance of microbiome–host homeostasis. This systematic review aims at analyzing how gut microbiome and host immune system influence each other during HIV pathogenesis. An online search applying the PubMed database was conducted. The number of total results (n = 35) was narrowed down to 5 relevant studies focusing on the interaction between the host and gut microbiome, whereas strict exclusion criteria were applied, thereby assuring that no other comorbidities impacted study results. Our analyses revealed that gut microbiome diversity correlated positively with CD4+ T cell counts and negatively with microbial translocation markers. However, quantitative changes in bacterial richness did not consistently correlate with the numbers of metabolically active bacterial populations. Despite the reported increase in potentially pathogenic bacteria and, conversely, decrease in protective populations, the gut microbiota exhibited immune-modulating qualities given that mucosal inflammatory sequelae were dampened by decreasing pro-inflammatory and accelerating anti-inflammatory cytokine responses. Future research is needed to further elucidate these findings, to gain a deeper insight into host–microbiota interactions and to develop novel therapeutic strategies.
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spelling pubmed-56327432017-10-13 Changes of the Intestinal Microbiome–Host Homeostasis in HIV-Infected Individuals – A Focus on the Bacterial Gut Microbiome Ribeiro, Ana Beatriz Dein Terra Mota Heimesaat, Markus M. Bereswill, Stefan Eur J Microbiol Immunol (Bp) Review Article Human immunodeficiency virus (HIV) infections cause severe CD4+ T cell depletion leading to chronic inflammation and immune activation, impaired barrier function, and microbial translocation. Even under effective antiretroviral therapy, these processes persist, leading to gut microbiome dysbiosis and disturbance of microbiome–host homeostasis. This systematic review aims at analyzing how gut microbiome and host immune system influence each other during HIV pathogenesis. An online search applying the PubMed database was conducted. The number of total results (n = 35) was narrowed down to 5 relevant studies focusing on the interaction between the host and gut microbiome, whereas strict exclusion criteria were applied, thereby assuring that no other comorbidities impacted study results. Our analyses revealed that gut microbiome diversity correlated positively with CD4+ T cell counts and negatively with microbial translocation markers. However, quantitative changes in bacterial richness did not consistently correlate with the numbers of metabolically active bacterial populations. Despite the reported increase in potentially pathogenic bacteria and, conversely, decrease in protective populations, the gut microbiota exhibited immune-modulating qualities given that mucosal inflammatory sequelae were dampened by decreasing pro-inflammatory and accelerating anti-inflammatory cytokine responses. Future research is needed to further elucidate these findings, to gain a deeper insight into host–microbiota interactions and to develop novel therapeutic strategies. Akadémiai Kiadó 2017-08-19 /pmc/articles/PMC5632743/ /pubmed/29034105 http://dx.doi.org/10.1556/1886.2017.00016 Text en © 2017, The Author(s) http://creativecommons.org/licenses/by-nc/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 International License (https://creativecommons.org/licenses/by-nc/4.0/), which permits unrestricted use, distribution, and reproduction in any medium for non-commercial purposes, provided the original author and source are credited, a link to the CC License is provided, and changes – if any – are indicated.
spellingShingle Review Article
Ribeiro, Ana Beatriz Dein Terra Mota
Heimesaat, Markus M.
Bereswill, Stefan
Changes of the Intestinal Microbiome–Host Homeostasis in HIV-Infected Individuals – A Focus on the Bacterial Gut Microbiome
title Changes of the Intestinal Microbiome–Host Homeostasis in HIV-Infected Individuals – A Focus on the Bacterial Gut Microbiome
title_full Changes of the Intestinal Microbiome–Host Homeostasis in HIV-Infected Individuals – A Focus on the Bacterial Gut Microbiome
title_fullStr Changes of the Intestinal Microbiome–Host Homeostasis in HIV-Infected Individuals – A Focus on the Bacterial Gut Microbiome
title_full_unstemmed Changes of the Intestinal Microbiome–Host Homeostasis in HIV-Infected Individuals – A Focus on the Bacterial Gut Microbiome
title_short Changes of the Intestinal Microbiome–Host Homeostasis in HIV-Infected Individuals – A Focus on the Bacterial Gut Microbiome
title_sort changes of the intestinal microbiome–host homeostasis in hiv-infected individuals – a focus on the bacterial gut microbiome
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5632743/
https://www.ncbi.nlm.nih.gov/pubmed/29034105
http://dx.doi.org/10.1556/1886.2017.00016
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