Interplay Between Human Gut Bacteria and in the Occurrence of Neuropsychiatric Disorders in Mice.

To understand the roles of human gut bacteria in the occurrence of neuropsychiatric disorders, we isolated inflammatory K1 and anti-inflammatory from healthy human feces and examined their effects on the occurrence of altered microbiota, cognitive decline, and depression in mice. Oral gavage of K1 caused colitis, cognitive decline, and depression in mice in the elevated plus maze, tail suspension, and forced swimming tasks. However, NK41 treatment reduced K1-induced cognitive decline and anxiety/depression. Furthermore, NK41 treatment increased K1-suppressed brain-derived neurotrophic factor (BDNF) expression and BDNF/NeuN cell population and suppressed K1-induced NF-κB activation and LPS/Iba1 and NF-κB/Iba1 (microglial) cell populations in the hippocampus. NK41 treatment also suppressed K1-induced TNF-α and LPS levels in the blood and TNF-α expression, myeloperoxidase activity, NF-κB/CD11c and CD11b/CD11c cell populations in the colon. Furthermore, NK41 treatment decreased K1-induced colonic MUC2 expression, gut Proteobacteria population, and fecal LPS levels and modified the bacterial abundance related to polysaccharide breaking and biosynthesis. In conclusion, the overgrowth of inflammatory bacteria such as in the gastrointestinal tract can cause neuropsychiatric disorders with gut microbiota alteration and the superiority of anti-inflammatory bacteria such as can alleviate neuropsychiatric disorders with the attenuation of altered microbiota.