Abstract
Intestinal motility disorders represent a significant pathological feature of various gastrointestinal conditions, involving intricate interactions among the enteric nervous system (ENS), microbial communities, and the immune system. Antibiotic usage disrupts this delicate balance, leading to intestinal motility disorders. To address this issue, the present study was based on the antibiotic-induced intestinal motility disorders mouse model, and interventions were performed using Bifidobacterium bifidum BB1, BB7, BB8, and CCFM1391. Our findings demonstrate that CCFM1391 significantly reduces intestinal transit time and fecal water content, which ameliorates abnormal intestinal motility (P < 0.01). It was shown that Bifidobacterium bifidum CCFM1391 had the most significant effect in regulating intestinal motility disorders, and therefore was selected as the subject for further investigation. Further exploration of its mechanism of action revealed that CCFM1391 adjusted the structure of intestinal flora (significantly increased the abundance of Akkermansia) (P < 0.0001), enhances short-chain fatty acids (SCFAs) production (acetic acid, propionic acid, isovaleric acid) (P < 0.05), and stimulates serotonin (5-HT) release (P < 0.0001), thereby activating the 5-HT4 receptor pathway to restore enteric nerve function. Additionally, CCFM1391 strengthens the intestinal barrier by upregulating tight junction proteins (Occludin, Claudin-1, ZO-1) (P < 0.01) and modulating inflammatory responses—reducing pro-inflammatory factors (CXCL-1, IL-17) and increasing anti-inflammatory factors (TGF-β) (P < 0.01). These results underscore CCFM1391's efficacy in alleviating antibiotic-induced intestinal motility disorders through modulation of gut microbiota and their metabolites, and by influencing neuro-epithelial-immune interactions. This study provides a theoretical basis for probiotic interventions and highlights their potential clinical applications.
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