The effect of diet on hypertensive pathology: is there a link via gut microbiota-driven immunometabolism?


Journal

Cardiovascular research
ISSN: 1755-3245
Titre abrégé: Cardiovasc Res
Pays: England
ID NLM: 0077427

Informations de publication

Date de publication:
01 07 2019
Historique:
received: 15 11 2018
revised: 07 02 2019
accepted: 03 04 2019
pubmed: 6 4 2019
medline: 17 6 2020
entrez: 6 4 2019
Statut: ppublish

Résumé

Over the past decade, the immune system has emerged as an important component in the aetiology of hypertension. There has been a blooming interest in the contribution of the gut microbiota, the microbes that inhabit our small and large intestine, to blood pressure (BP) regulation. The gastrointestinal tract houses the largest number of immune cells in our body, thus, it is no surprise that its microbiota plays an important functional role in the appropriate development of the immune system through a co-ordinated sequence of events leading to immune tolerance of commensal bacteria. Importantly, recent evidence supports that the gut microbiota can protect or promote the development of experimental hypertension and is likely to have a role in human hypertension. One of the major modulators of the gut microbiota is diet: diets that emphasize high intake of fermentable fibre, such as the Mediterranean diet and the Dietary Approaches to Stop Hypertension, promote expansion of protective microbes that release gut metabolites such as short-chain fatty acids, which are immune-, BP-, and cardio-protective, likely acting through G-coupled protein receptors. In contrast, diets lacking fibre or high in salt and fat, such as the Western diet, reduce prevalence of commensal microbial species and support a pathogenic and pro-inflammatory environment, including the release of the pro-atherosclerotic trimethylamine N-oxide. Here, we review the current understanding of the gut microbiota-driven immune dysfunction in both experimental and clinical hypertension, and how these changes may be addressed through dietary interventions.

Identifiants

pubmed: 30951169
pii: 5429355
doi: 10.1093/cvr/cvz091
doi:

Types de publication

Journal Article Research Support, Non-U.S. Gov't Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

1435-1447

Informations de copyright

Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2019. For permissions, please email: journals.permissions@oup.com.

Auteurs

Hamdi A Jama (HA)

Heart Failure Research Group, Baker Heart and Diabetes Institute, 75 Commercial Rd, Melbourne, VIC, Australia.
Hypertension Research Laboratory, School of Biological Sciences, Faculty of Science, Monash University, 25 Rainforest Walk, Clayton, Melbourne, VIC, Australia.

Anna Beale (A)

Heart Failure Research Group, Baker Heart and Diabetes Institute, 75 Commercial Rd, Melbourne, VIC, Australia.

Waled A Shihata (WA)

Heart Failure Research Group, Baker Heart and Diabetes Institute, 75 Commercial Rd, Melbourne, VIC, Australia.

Francine Z Marques (FZ)

Heart Failure Research Group, Baker Heart and Diabetes Institute, 75 Commercial Rd, Melbourne, VIC, Australia.
Hypertension Research Laboratory, School of Biological Sciences, Faculty of Science, Monash University, 25 Rainforest Walk, Clayton, Melbourne, VIC, Australia.

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Classifications MeSH