Social defeat stress induced dysbiosis of gut microbiota and its attenuation via Lactobacillus plantarum treatment

Abstract

It is well known that the activation of the sympathetic nervous system and Hypothalamic-Pituitary-Adrenal (HPA) axis induced by a stressor affects many aspects of gastrointestinal tract functions such as GI motility, mucus secretion, and intestinal immune responses. We investigated the effect of social defeat stress on the gut microbiota, their metabolic functions, and hosts responses. In addition, we further investigated whether probiotics could prevent such changes. C57BL/6 mice were treated with Lactobacillus plantarum in the form of food pellet for 4 weeks, after which mice were exposed to a social defeat stress for a week. Host side responses were analyzed by qRT-PCR and ELISA, while the gut microbiome was analyzed via sequencing of V4-5 region of 16s rRNA. We observed that exposure to stress alters gut microbiome structure, its metabolic function and hosts physiology which were effectively prevented by L. plantarum treatment. Here, we characterized bacterial and metabolic components which may deteriorate the symptoms of stress-induced depression through affecting hosts serotonergic and immunogenic response. In particular, abundances of Anaerosipes spp., Helicobateraceae, Mogibacteriaceae, Prevotella spp., Suterrella spp., Christensenella spp., and Parabacteroides spp. were significantly increased in response to social defeat stress and fully prevented through L. plantarum treatment. Furthermore, microbial metabolic pathways, including glycan biosynthesis were altered in response to the stress exposure. Increased level of LPS may contributes to evoke pro-inflammatory responses which eventually affects hosts serotonin biosynthesis. These changes were also effectively prevented through the treatment of L.plantarum. Here, this study reports a beneficial effect of Lactobacillus plantarum in host stress resilience and potential microbial-metabolic components (psycho-pathogens) which affect the pathogenesis of stress induced mental illness.