Bifidobacterium lactis BL-99 protects mice with osteoporosis caused by colitis via gut inflammation and gut microbiota regulation

• Published in: Food & function Vol. 13; no. 3; pp. 1482 - 1494
• Main Authors: Lan, Hui, Liu, Wei-Hsien, Zheng, Hanying, Feng, Haotian, Zhao, Wen, Hung, Wei-Lian, Li, Hongwei
• Format: Journal Article
• Language: English
• Published: England Royal Society of Chemistry 07.02.2022
• Subjects: Animals; Bifidobacterium; Bifidobacterium lactis; Biomedical materials; Bone loss; Colitis, Ulcerative - complications; Colitis, Ulcerative - prevention & control; Colon; Computed tomography; Cytokines; Dextran; Dextran Sulfate; Dextrans; Dietary supplements; Digestive system; Disease Models, Animal; Dysbacteriosis; Gastrointestinal Microbiome - drug effects; Gastrointestinal tract; IL-1β; Inflammatory bowel disease; Inflammatory bowel diseases; Injury analysis; Injury prevention; Interleukin 17; Interleukin 6; Intestinal microflora; Intestine; Male; Mice; Mice, Inbred C57BL; Microbiota; Microenvironments; Molecular modelling; Osteoporosis; Osteoporosis - complications; Patients; Probiotics; Probiotics - pharmacology; Sodium sulfate; Specific Pathogen-Free Organisms; Tumor necrosis factor-α; Ulcerative colitis; Weight loss; Zonula occludens-1 protein
• ISSN: 2042-6496; 2042-650X
• DOI: 10.1039/d1fo02218k

Patients diagnosed with inflammatory bowel disease or related conditions also frequently suffer from osteoporosis as a consequence of changes in the intestinal microenvironment and consequent dysbiosis. We hypothesized that anti-inflammatory probiotic treatment would be sufficient to alleviate intestinal inflammation and thereby prevent the development of osteoporosis. To that end, the ability of BL-99 administration to protect against bone loss in an experimental model of dextran sodium sulfate-induced ulcerative colitis (UC) was analyzed, and the underlying molecular mechanisms were interrogated in detail. The results of these analyses revealed that BL-99 administration suppressed colitis-associated weight loss ( < 0.05), disease activity index scores, and the production of proinflammatory cytokines (TNF-α, IL-1β, IL-6, and IL-17) ( < 0.05). Colon tissue pathological sections similarly revealed BL-99-mediated reductions in tissue injury severity. Micro-computed tomography (Micro-CT) analyses further exhibited significant improvements in percent bone volume (BV/TV) as well as trabecular number and thickness in BL-99-treated animals ( < 0.05). Such probiotic supplementation also resulted in pronounced changes in the composition of the gut microbiota. Moreover, BL-99 intervention markedly increased the expression of intestinal barrier-related proteins (Claudin-1, MUC2, ZO-1, and Occludin). Together, these results suggest that BL-99 can be utilized as a beneficial probiotic preparation to prevent the incidence of osteoporosis in UC patients owing to its ability to shape the intestinal microflora and to suppress inflammatory cytokine production.