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The Probiotic Lactobacillus fermentum Prevents Dysbiosis and Vascular Oxidative Stress in Rats with Hypertension Induced by Chronic Nitric Oxide Blockade
Author(s) -
RoblesVera Iñaki,
Toral Marta,
la Visitación Néstor,
Sánchez Manuel,
Romero Miguel,
Olivares Mónica,
Jiménez Rosario,
Duarte Juan
Publication year - 2018
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201800298
Subject(s) - lactobacillus fermentum , oxidative stress , dysbiosis , nitric oxide , endothelial dysfunction , inflammation , medicine , bifidobacterium breve , immunology , pharmacology , gut flora , nitric oxide synthase , probiotic , endocrinology , lactobacillus , bifidobacterium , chemistry , biology , biochemistry , bacteria , lactic acid , lactobacillus plantarum , genetics , fermentation
Scope Whether the probiotic Lactobacillus fermentum CECT5716 (LC40) ameliorates hypertension in rats with chronic nitric oxide (NO) synthase inhibition is tested. Methods and results Rats are randomly divided into four different groups and treated for 4 weeks: a) vehicle (control), b) vehicle plus N G ‐nitro‐ l ‐arginine methyl ester ( l ‐NAME; 50 mg 100 mL −1 in drinking water), c) LC40 (10 9 colony‐forming units d –1 by gavage), and d) LC40 plus l ‐NAME. l ‐NAME induces gut dysbiosis, characterized mainly by an increased Fimicutes/Bacteroidetes (F/B) ratio and reduced Bifidobacterium content, increased Th17 cells and reduced Treg in mesenteric lymph nodes (MLN), increased aortic Th17 infiltration and reactive oxygen species, reduced aortic endothelium‐dependent relaxant response to acetylcholine, and hypertension. LC40 prevents gut dysbiosis, alters the Th17/Treg balance in MLN, vascular oxidative stress, and inflammation, slightly improves endothelial dysfuncion but do not inhibit the development of l ‐NAME‐induced hypertension. Conclusion Chronic LC40 treatment, in this model of chronic inhibition of NO synthesis, reduces early events involved in atherosclerosis development, such as vascular oxidative stress and pro‐inflammatory status, as a result of prevention of gut dysbiosis and immune changes in MLN, but not hypertension, confirming the critical role of NO in the antihypertensive effects of LC40 in genetic hypertension.