Dietary salt promotes neurovascular and cognitive dysfunction through a gut-initiated TH17 response Academic Article uri icon

Overview

MeSH Major

  • Brain
  • Dendritic Cells
  • Dysbiosis
  • Gastrointestinal Microbiome
  • Infarction, Middle Cerebral Artery
  • Intestines
  • Receptors, Antigen, T-Cell, gamma-delta
  • T-Lymphocytes

abstract

  • A diet rich in salt is linked to an increased risk of cerebrovascular diseases and dementia, but it remains unclear how dietary salt harms the brain. We report that, in mice, excess dietary salt suppresses resting cerebral blood flow and endothelial function, leading to cognitive impairment. The effect depends on expansion of TH17 cells in the small intestine, resulting in a marked increase in plasma interleukin-17 (IL-17). Circulating IL-17, in turn, promotes endothelial dysfunction and cognitive impairment by the Rho kinase-dependent inhibitory phosphorylation of endothelial nitric oxide synthase and reduced nitric oxide production in cerebral endothelial cells. The findings reveal a new gut-brain axis linking dietary habits to cognitive impairment through a gut-initiated adaptive immune response compromising brain function via circulating IL-17. Thus, the TH17 cell-IL-17 pathway is a putative target to counter the deleterious brain effects induced by dietary salt and other diseases associated with TH17 polarization.

publication date

  • January 15, 2018

Research

keywords

  • Academic Article

Identity

Language

  • eng

Digital Object Identifier (DOI)

  • 10.1038/s41593-017-0059-z

PubMed ID

  • 29335605

Additional Document Info

start page

  • 1

end page

  • 10