Effect of heat-inactivated N1115 on microbiota and gut-brain axis related molecules.

This study was conducted to evaluate the possibility of using heated-inactivated lactobacilli to protect neonates from harmful effects of antibiotics. Thirty neonate mice were randomly divided into three groups of ten and treated with either sterilized water, an antibiotics cocktail, or the same antibiotics plus heat-inactivated N1115. The administration of antibiotics significantly increased the serum interleukin-6 (IL-6) levels of the tested mice (p<0.01, p<0.001, respectively) and decreased their serum corticosterone levels (p<0.01, p<0.01, respectively). The colonic crypts were significantly less deep in mice treated with antibiotics and with antibiotics plus N1115 (p<0.05). Antibiotics caused significantly abnormal expression of brain-derived neurotrophic factor (BDNF), γ-aminobutyric acid type A receptor α1 (GABA), γ-aminobutyric acid type B receptor1 (GABA), and 5-hydroxytryptamine receptor1A (5-HT) in the hippocampus (p<0.05, p<0.01, p<0.01, respectively) and of GABA in the prefrontal cortex (p<0.01). Heat-inactivated lactobacilli alleviated these abnormal changes. Antibiotics greatly decreased the Shannon index of the fecal microbiota and significantly increased the number of (p<0.001), with fewer and (p<0.05). Antibiotics not only cause microbiota dysbiosis, but also cause abnormal changes in important molecules in the gut-brain axis. All these abnormal changes are alleviated by heat-inactivated N1115. This indicates that heat-inactivated N1115 has a certain improvement effect on changes caused by antibiotics.