Recent studies reported that the impairment of gut microbiota (Dysbiosis) cause impairments of gut metabolisms, which induce chronic inflammation in the body. High salt intake not only increases blood pressure, but also causes Dysbiosis. However, the detailed mechanism has not been clarified yet. Here we investigate the mechanism of the atherosclerosis progression through dysbiosis caused by high salt diet. 16-week-old male Apolipoprotein E-deficient (ApoE-/-) mice were fed normal breeding diet (ND group), high-fat high-sucrose diet (HFHSD group), and high-fat high-sucrose high-salt diet (HFHSDNaCl8%, high salt group) for 8 weeks. The concentration of salt in ND and HFHSD is set as 2%. Immune cells in the aorta were extracted and evaluated by FACS CANTII. The metagenome was evaluated by the 16S target sequencing method. Lipidome in the aorta, serum, or intestinal contents were evaluated and quantified by GCMS system (Agilent 7890B/5977B). In high salt group, gene expression levels of inflammatory cytokines and chemokines were upregulated, and M1 macrophages and Group 2 innate lymphoid cells in atherosclerotic lesions increased. The prevalence of Firmicutes decreased and the prevalence of Bacteroidetes increased. Lipidome in the aorta, serum and intestinal contents were significantly different among the HFHSD group and high salt group, although the lipids administered were the same. High salt intake increases M1 macrophages and Group 2 innate lymphoid cells by altering intestinal bacterial lipid metabolisms, and could deteriorate chronic inflammation of arteriosclerosis.
T. Kimura: None. Y. Hashimoto: None. T. Senmaru: None. E. Ushigome: None. M. Hamaguchi: None. M. Yamazaki: None. M. Fukui: None.