Targeting the gut microbiota to investigate the mechanism of Lactiplantibacillus plantarum 1201 in negating colitis aggravated by a high-salt diet

High-salt diet (HSD) affects the composition and function of the intestinal microbiota and cause health problems. This study confirmed that HSD aggravates dextran sulphate sodium (DSS)-induced colitis by changing the relative abundance of the gut microbiota, activating the NF-kappa B pathway, and up-regulating the mRNA levels of inflammatory factors. We explored the effect of L. plantarum 1201 in negating DSS-induced ulcerative colitis, which is aggravated by HSD for the first time. Results show that L. plantarum 1201 rebuilt the balance of intestinal flora by decreasing the ratio of Firmicutes/Bacteroidetes and increasing the relative abundance of Bifidobacterium, Lactobacillus and butyric-producing bacteria. Moreover, L. plantarum 1201 inhibited the upregulation of inflammatory cytokines (e.g., IL-1 beta, TNF-alpha, IL-6, IL-22, and IFN-gamma) mRNA levels, increased colonic tight junction protein (ZO-1, ocludin, and claudin-3) expression, and increased serum levels of beneficial metabolites, including alpha-tocopherol (alpha-T) and D-mannose. By reconstructing an animal model of colitis, we further discovered that alpha-T and D-mannose inhibited the NF-kappa B pathway, improved tissue injury, and decreased the expression of pro-inflammatory cytokines (e.g., IL-1 beta, TNF-alpha, and IL-6). This study proves for the first time that L. plantarum 1201 attenuates high-salt-aggravated colitis by increasing the serum concentrations of endogenic D-mannose in mice serum and inhibiting the consumption of alpha-T through intestinal flora. Therefore, regulating the gut microbiota is a potential treatment for high-salt-aggravated colitis.