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Salmonella Typhimurium is widely distributed in food. It can colonise the gastrointestinal tract after ingestion, causing lamina propria edema, inflammatory cell infiltration, and mucosal epithelial decomposition. A high-fat diet (HFD) can induce an inflammatory response, but whether HFD can increase the infection level of S. Typhimurium is unknown. We established a model of Salmonella enterica subsp. enterica serovar Typhimurium strain ATCC 13311 ATCC 13311 infection in healthy adult mice with a maintenance diet (MD) or HFD to explore the effect of Lactiplantibacillus plantarum 1201 intervention on S. Typhimurium ATCC 13311 colonization and its protective effects on mice. HFD exacerbated the infection of S. Typhimurium ATCC 13311, while the intervention of L. plantarum 1201 effectively mitigated this process. L. plantarum 1201 can reduce the colonies of S. ATCC 13311 in the intestines and tissues; and reduce intestinal inflammation by down-regulating the level of TLR4/NF-κB pathway related proteins in serum and the expression of related inflammatory factors in the colon and jejunum. Since L. plantarum 1201 can inhibit the colonization of S. Typhimurium ATCC 13311 and relieve inflammation in HFD, current research may support the use of L. plantarum 1201 to prevent S. Typhimurium infection.

[Display omitted] • HSD aggravated colitis by disturbing gut microbiota and activating NF- κ B pathway. • L. plantarum 1201 alleviated colitis through partially restoring intestinal flora. • 1201 increased serum levels of α-T and D-mannose through intestinal flora metabolism. • α-T and D-mannose alleviated colitis through modulating intestinal immune function. 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-κB 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 up-regulation of inflammatory cytokines (e.g., IL-1β, TNF-α, IL-6, IL-22, and IFN-γ) mRNA levels, increased colonic tight junction protein (ZO-1, ocludin, and claudin-3) expression, and increased serum levels of beneficial metabolites, including alpha-tocopherol (α-T) and D-mannose. By reconstructing an animal model of colitis, we further discovered that α-T and D-mannose inhibited the NF-κB pathway, improved tissue injury, and decreased the expression of pro-inflammatory cytokines (e.g., IL-1β, TNF-α, 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 α-T through intestinal flora. Therefore, regulating the gut microbiota is a potential treatment for high-salt-aggravated colitis. [ABSTRACT FROM AUTHOR]

Salmonella Typhimurium is widely distributed in food. It can colonise the gastrointestinal tract after ingestion, causing lamina propria edema, inflammatory cell infiltration, and mucosal epithelial decomposition. A high-fat diet (HFD) can induce an inflammatory response, but whether HFD can increase the infection level of S. Typhimurium is unknown. We established a model of Salmonella enterica subsp. enterica serovar Typhimurium strain ATCC 13311 ATCC 13311 infection in healthy adult mice with a maintenance diet (MD) or HFD to explore the effect of Lactiplantibacillus plantarum 1201 intervention on S. Typhimurium ATCC 13311 colonization and its protective effects on mice. HFD exacerbated the infection of S. Typhimurium ATCC 13311, while the intervention of L. plantarum 1201 effectively mitigated this process. L. plantarum 1201 can reduce the colonies of S. ATCC 13311 in the intestines and tissues; and reduce intestinal inflammation by down-regulating the level of TLR4/NF-κB pathway related proteins in serum and the expression of related inflammatory factors in the colon and jejunum. Since L. plantarum 1201 can inhibit the colonization of S. Typhimurium ATCC 13311 and relieve inflammation in HFD, current research may support the use of L. plantarum 1201 to prevent S. Typhimurium infection. [ABSTRACT FROM AUTHOR]

Salmonella Typhimurium is widely distributed in food. It can colonise the gastrointestinal tract after ingestion, causing lamina propria edema, inflammatory cell infiltration, and mucosal epithelial decomposition. A high-fat diet (HFD) can induce an inflammatory response, but whether HFD can increase the infection level of S. Typhimurium is unknown. We established a model of Salmonella enterica subsp. enterica serovar Typhimurium strain ATCC 13311 ATCC 13311 infection in healthy adult mice with a maintenance diet (MD) or HFD to explore the effect of Lactiplantibacillus plantarum 1201 intervention on S. Typhimurium ATCC 13311 colonization and its protective effects on mice. HFD exacerbated the infection of S. Typhimurium ATCC 13311, while the intervention of L. plantarum 1201 effectively mitigated this process. L. plantarum 1201 can reduce the colonies of S. ATCC 13311 in the intestines and tissues; and reduce intestinal inflammation by down-regulating the level of TLR4/NF-κB pathway related proteins in serum and the expression of related inflammatory factors in the colon and jejunum. Since L. plantarum 1201 can inhibit the colonization of S. Typhimurium ATCC 13311 and relieve inflammation in HFD, current research may support the use of L. plantarum 1201 to prevent S. Typhimurium infection.