Participation of bacteria in our Microbiome that appear to enhance NaCl-induced hypertension

On numerous occasions before, these GEITP pages have detailed our increasing realization that the bacteria in our gut (i.e. our microbiome) cooperates with our host genes and enzymes through a large number of incredibly intimate interactions. The attached full paper and editorial represent just the latest breakthrough on this topic. High blood pressure is a leading cause of cardiovascular disease, and therefore represents pre­ventable deaths in the U.S. Hypertension is also an increasingly prevalent and costly health burden, worldwide. Blood-pressure con­trol in clnical studies is poorly understood; debate on blood pressure control includes understanding the contribution of dietary salt.

Average daily sodium intake in the U.S. is more than 3.4 grams (equivalent to 8.5 g of table salt) –– despite the fact that dietary guidelines recommend an intake of less than 2.3 g (5.8 g of salt). Many studies have shown that excess sodium intake raises blood pressure in a dose-dependent manner. However, there are inter-individual differences in blood-pressure response to salt, which are generally detected in fewer than half of all subjects. Likely sources of such vari­ability include genetics, dietary consumption of other nutrients such as potassium, and kidney dis­ease. Interestingly, responses to sodium intake are more pronounced if individuals already have high blood pressure.

In addition, high salt intake may drive autoimmunity by inducing T-helper-17 (TH17) cells, which are known also to contribute to hypertension. Induction of TH17 cells depends on the gut microbiome, but the effects of salt on the gut microbiome were not known until now. Authors [see attached] show, in mice, that high salt intake affects the gut bacteria, particularly by depleting Lactobacillus murinus. Consequently, treatment of mice with L. murinus prevented salt-induced aggravation of actively induced experimental autoimmune encephalomyelitis (inflammation of brain and spinal cord) and salt-sensitive hypertension by modulating TH17 cells. Consistent with these findings, a moderate high-salt challenge –– in a pilot study in humans –– decreased the intestinal survival of Lactobacillus spp., increased TH17 cells, and increased blood pressure. These findings thus demonstrate a connection between high salt intake and the gut–immune axis, and the data also highlight the gut microbiome as a potential therapeutic target for counteracting salt-sensitive conditions.

Nature 30 Nov 2o17; 551: 585–589 & News’N’View editorial pp 571–572

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