Alleviation of cognitive impairment by gut microbiota lipopolysaccharide production-suppressing Lactobacillus plantarum and Bifidobacterium longum in mice

Bacterial lipopolysaccharide (LPS) is a risk factor for the outbreak of Alzheimer's disease. Therefore, we isolated Lactobacillus plantarum NK151 and Bifidobacterium longum NK173 from a human fecal bacteria collection, which inhibited Escherichia coli LPS production, and examined their effects on the Escherichia coli K1- or LPS-induced cognitive impairment in mice. Oral gavage of NK151, NK173, or their (4 : 1) mixture (NKm) significantly alleviated Escherichia coli K1-induced cognitive impairment-like behaviors in the Y-maze and novel object recognition tasks. Their treatments decreased IL-1 beta, IL-6, and TNF-alpha expression and NF-kappa B+/Iba1(+) and LPS+/Iba1(+) cell populations in the hippocampus, while the brain-derived neurotrophic factor (BDNF)(+)/neuronal nuclei (NeuN)(+) cell population and BDNF to proBNDF expression increased. They suppressed LPS-induced cognition impairment-like behaviors and neuroinflammation marker levels in the hippocampus. Treatment with them reduced Escherichia coli K1- or LPS-induced LPS and apolipoprotein E levels in the blood and inflammatory marker levels in the colon. Furthermore, treatment with them modulated fecal Proteobacteria, Bacteroidetes, and Verrucomicrobia populations. Of these gut bacteria, Bacteroidaceae, Odoribacteraceae, Lactobacillaceae, Bifidobacteriaceae, Rikenellaceae, Helicobacteraceae, and Deferribacteraceae are correlated with cognitive function and blood and fecal LPS levels. These findings suggest that NK151 and NK173 may alleviate cognitive impairment with colitis by upregulating NF-kappa B-mediated BDNF expression through the suppression of fecal and blood bacterial LPS levels.

Automated summary

The study suggests that NK151 and NK173 may alleviate cognitive impairment with colitis by upregulating NF-kappa B-mediated BDNF expression through the suppression of fecal and blood bacterial LPS levels.