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The Gut Microbiome, Inflammation, and Salt-Sensitive Hypertension

Authors
  • Elijovich, Fernando1
  • Laffer, Cheryl L.1
  • Sahinoz, Melis2
  • Pitzer, Ashley1
  • Ferguson, Jane F.2
  • Kirabo, Annet1, 3
  • 1 Vanderbilt University Medical Center, Room 536 Robinson Research Building, Nashville, TN, 37232-6602, USA , Nashville (United States)
  • 2 Vanderbilt University Medical Center, Nashville, TN, USA , Nashville (United States)
  • 3 Vanderbilt University School of Medicine, Nashville, TN, USA , Nashville (United States)
Type
Published Article
Journal
Current Hypertension Reports
Publisher
Springer-Verlag
Publication Date
Sep 03, 2020
Volume
22
Issue
10
Identifiers
DOI: 10.1007/s11906-020-01091-9
Source
Springer Nature
Keywords
License
Green

Abstract

Purpose of ReviewSalt sensitivity of blood pressure (SSBP) is an independent predictor of death due to cardiovascular events and affects nearly 50% of the hypertensive and 25% of the normotensive population. Strong evidence indicates that reducing sodium (Na+) intake decreases blood pressure (BP) and cardiovascular events. The precise mechanisms of how dietary Na+ contributes to elevation and cardiovascular disease remain unclear. The goal of this review is to discuss mechanisms of salt-induced cardiovascular disease and how the microbiome may play a role.Recent FindingsThe innate and adaptive immune systems are involved in the genesis of salt-induced hypertension. Mice fed a high-salt diet exhibit increased inflammation with a marked increase in dendritic cell (DC) production of interleukin (IL)-6 and formation of isolevuglandins (IsoLG)-protein adducts, which drive interferon-gamma (IFN-γ) and IL-17A production by T cells. While prior studies have mainly focused on the brain, kidney, and vasculature as playing a role in salt-induced hypertension, the gut is the first and largest location for Na+ absorption. Research from our group and others strongly suggests that the gut microbiome contributes to salt-induced inflammation and hypertension.SummaryRecent studies suggest that alterations in the gut microbiome contribute to salt-induced hypertension. However, the contribution of the microbiome to SSBP and its underlying mechanisms are not known. Targeting the microbiota and the associated immune cell activation could conceivably provide the much-needed therapy for SSBP.

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