Neurobiota Research Center, Department of Life and Nanopharmaceutical Sciences, College of Pharmacy, Kyung Hee University, Kyungheedae-ro, Dongdaemun-gu, Seoul 02447, Korea.
Nutrients. 2019 Apr 11;11(4):819. doi: 10.3390/nu11040819.
The gut dysbiosis by stressors such as immobilization deteriorates psychiatric disorders through microbiota-gut-brain axis activation. To understand whether probiotics could simultaneously alleviate anxiety/depression and colitis, we examined their effects on immobilization stress (IS)-induced anxiety/depression and colitis in mice. The probiotics NK33 and NK98 were isolated from healthy human feces. Mice with anxiety/depression and colitis were prepared by IS treatment. NK33 and NK98 potently suppressed NF-κB activation in lipopolysaccharide (LPS)-induced BV-2 cells. Treatment with NK33 and/or NK98, which were orally gavaged in mice before or after IS treatment, significantly suppressed the occurrence and development of anxiety/depression, infiltration of Iba1⁺ and LPS⁺/CD11b⁺ cells (activated microglia) into the hippocampus, and corticosterone, IL-6, and LPS levels in the blood. Furthermore, they induced hippocampal BDNF expression while NF-κB activation was suppressed. NK33 and/or NK98 treatments suppressed IS-induced colon shortening, myeloperoxidase activity, infiltration of CD11b⁺/CD11c⁺ cells, and IL-6 expression in the colon. Their treatments also suppressed the IS-induced fecal Proteobacteria population and excessive LPS production. They also induced BDNF expression in LPS-induced SH-SY5Y cells in vitro. In conclusion, NK33 and NK98 synergistically alleviated the occurrence and development of anxiety/depression and colitis through the regulation of gut immune responses and microbiota composition.
应激引起的肠道菌群失调通过微生物群-肠-脑轴的激活恶化精神疾病。为了了解益生菌是否可以同时缓解焦虑/抑郁和结肠炎，我们研究了它们对束缚应激（IS）诱导的焦虑/抑郁和结肠炎小鼠的影响。益生菌 NK33 和 NK98 从健康人的粪便中分离出来。通过 IS 处理制备具有焦虑/抑郁和结肠炎的小鼠。NK33 和 NK98 强烈抑制脂多糖（LPS）诱导的 BV-2 细胞中 NF-κB 的激活。在 IS 处理之前或之后用 NK33 和/或 NK98 口服灌胃处理，显著抑制焦虑/抑郁的发生和发展、Iba1⁺ 和 LPS⁺/CD11b⁺ 细胞（活化的小胶质细胞）浸润到海马体中，以及血液中的皮质酮、IL-6 和 LPS 水平。此外，它们诱导海马体 BDNF 表达，同时抑制 NF-κB 激活。NK33 和/或 NK98 处理抑制 IS 诱导的结肠缩短、髓过氧化物酶活性、CD11b⁺/CD11c⁺ 细胞浸润和结肠中 IL-6 的表达。它们的处理还抑制了 IS 诱导的粪便变形菌种群和过量 LPS 产生。它们还在体外诱导 LPS 诱导的 SH-SY5Y 细胞中 BDNF 表达。总之，NK33 和 NK98 通过调节肠道免疫反应和微生物群落组成，协同缓解焦虑/抑郁和结肠炎的发生和发展。
