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Salt-responsive gut commensal modulates TH17 axis and disease

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TLDR
This paper showed that high salt intake affects the gut microbiome in mice, particularly by depleting Lactobacillus murinus, and treatment of mice with L. murinus prevented salt-induced aggravation of actively induced experimental autoimmune encephalomyelitis and salt-sensitive hypertension by modulating T helper 17 (TH17) cells.
Abstract
A Western lifestyle with high salt consumption can lead to hypertension and cardiovascular disease. High salt may additionally drive autoimmunity by inducing T helper 17 (TH17) cells, which can also contribute to hypertension. Induction of TH17 cells depends on gut microbiota; however, the effect of salt on the gut microbiome is unknown. Here we show that high salt intake affects the gut microbiome in mice, particularly by depleting Lactobacillus murinus. Consequently, treatment of mice with L. murinus prevented salt-induced aggravation of actively induced experimental autoimmune encephalomyelitis and salt-sensitive hypertension by modulating TH17 cells. In line with these findings, a moderate high-salt challenge in a pilot study in humans reduced intestinal survival of Lactobacillus spp., increased TH17 cells and increased blood pressure. Our results connect high salt intake to the gut-immune axis and highlight the gut microbiome as a potential therapeutic target to counteract salt-sensitive conditions.

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Exercise benefits in cardiovascular disease: beyond attenuation of traditional risk factors

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Robert C. Edgar
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TL;DR: The RDP Classifier can rapidly and accurately classify bacterial 16S rRNA sequences into the new higher-order taxonomy proposed in Bergey's Taxonomic Outline of the Prokaryotes, and the majority of the classification errors appear to be due to anomalies in the current taxonomies.
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What are the mechanisms by which Th17 cells contribute to diseases of the gut-brain axis?

The provided paper does not discuss the specific mechanisms by which Th17 cells contribute to diseases of the gut-brain axis.