| Summary: | Excessive expression of interleukin (IL)-1β in the brain causes depression and cognitive dysfunction. Herein, we investigated the effect of <i>Lactobacillus gasseri</i> NK109, which suppressed IL-1β expression in activated macrophages, on <i>Escherichia coli</i> K1-induced cognitive impairment and depression in mice. Germ-free and specific pathogen-free mice with neuropsychiatric disorders were prepared by oral gavage of K1. NK109 alleviated K1-induced cognition-impaired and depressive behaviors, decreased the expression of IL-1β and populations of NF-κB<sup>+</sup>/Iba1<sup>+</sup> and IL-1R<sup>+</sup> cells, and increased the K1-suppressed population of BDNF<sup>+</sup>/NeuN<sup>+</sup> cells in the hippocampus. However, its effects were partially attenuated by celiac vagotomy. NK109 treatment mitigated K1-induced colitis and gut dysbiosis. Tyndallized NK109, even if lysed, alleviated cognitive impairment and depression. In conclusion, NK109 alleviated neuropsychiatric disorders and colitis by modulating IL-1β expression, gut microbiota, and vagus nerve-mediated gut–brain signaling.
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