Dysbiosis leads to continuous progress of inflammatory bowel disease (IBD). However, current therapeutic approaches for IBD have limited efficacy and are associated with various side effects. This study focused on exploring the positive effect of a new Bacillus cereus (B. cereus) strain (HMPM18123) in a colitis mouse model and elucidate the underlying molecular mechanisms. The colitis symptoms were alleviated by the B. cereus administration as evidenced by decreased body weight loss, colon length shortening, disease activity index score, and histopathological score. The B. cereus mitigated intestinal epithelial barrier damage by upregulating tight junction protein expression. Moreover, B. cereus exerted anti-inflammatory effects by regulating macrophage polarization and suppressing the TLR4-NF-κB-NLRP3 inflammasome signaling pathways. B. cereus also rebalanced the damaged gut microbiota. Thus, the molecular mechanism of alleviating colitis by B. cereus treatment involved the regulation of the TLR4-NF-κB-NLRP3 inflammasome signaling pathways in intestinal mucosal barriers by modulating gut microbiota composition.

中文翻译：

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益生菌蜡样芽孢杆菌通过改善肠道屏障功能、抗炎和调节肠道微生物群来缓解葡聚糖硫酸钠诱导的小鼠结肠炎

生态失调导致炎症性肠病 (IBD) 的持续发展。然而，目前 IBD 的治疗方法疗效有限，并伴有各种副作用。本研究的重点是探索一种新的蜡状芽孢杆菌( B. cereus ) 菌株 (HMPM18123) 在结肠炎小鼠模型中的积极作用，并阐明潜在的分子机制。结肠炎症状通过施用蜡状芽孢杆菌得到缓解，如体重减轻减少、结肠长度缩短、疾病活动指数评分和组织病理学评分所证明。的蜡状芽孢杆菌通过上调紧密连接蛋白的表达减轻肠上皮屏障的损坏。此外，蜡状芽孢杆菌通过调节巨噬细胞极化和抑制 TLR4-NF-κB-NLRP3 炎症小体信号通路发挥抗炎作用。B. cereus还重新平衡了受损的肠道微生物群。因此，蜡状芽孢杆菌治疗缓解结肠炎的分子机制涉及通过调节肠道微生物群组成来调节肠粘膜屏障中的 TLR4-NF-κB-NLRP3 炎症小体信号通路。