Lactobacillus johnsonii CJLJ103 attenuates colitis and memory impairment in mice by inhibiting gut microbiota lipopolysaccharide production and NF-κB activation

Exposure to excessive lipopolysaccharide (LPS) by the gut microbiota disturbance causes ulcerative colitis and memory impairment. Therefore, we isolated anti-inflammatory Lactobacillus johnsonii CJLJ103 (LJ) from human fecal microbiota as an inhibitor for Escherichia coli growth and LPS production and investigated anti-colitic and memory impairment-ameliorating effects in mice. Oral administration of LJ inhibited 2,3,6-trinitrobenzenesulfonic acid (TNBS)-induced colon shortening, colonic myeloperoxidase activity, and NF-κB activation in mice. Furthermore, LJ inhibited TNBS-induced TNF and IL-1β expression in the colon but increased TNBS-suppressed expression of IL-10 and tight-junction proteins. Treatment with LJ inhibited fecal LPS levels and proteobacteria/bacteroidetes ratio in mice with TNBS-induced colitis. Furthermore, LJ ameliorated LPS-induced memory impairment in mice. LJ also suppressed LPS-induced NF-κB activation in the hippocampus and increased LPS-suppressed brain-derived neurotrophic factor expression. These findings suggest that LJ, a member of human gut microbiota, may ameliorate colitis and memory impairment, thereby acting as a useful probiotic.