![]() ![]() Citation12 Sex steroid deficiency leading to intestinal barrier dysfunction and subsequent increase in circulating lipopolysaccharides (LPS) and CD4+ T cells has been suggested as an important mechanism for the development of osteoporosis in postmenopausal women. In osteoimmunological studies, the balance of Th17/Treg and related inflammatory factors have been shown to be closely related to bone metabolism dysregulation. Citation11 Impairment of the intestinal barrier allows microorganisms to enter the subepithelial structures from the intestinal metastatic lumen, and trigger an inflammatory response. Citation9 Since intestinal epithelial cells are sealed by tight junction proteins (TJs), Citation10 such as ZO-1, claudin-1, and occludin, the intestinal microbiota can alter the expression and distribution of TJs, thus altering the permeability of the intestinal barrier. Citation7, Citation8 The intestinal epithelial barrier plays a crucial role in separating the internal structures from harmful antigens and pathogens and performing immune protective functions. Citation4–6 The gastrointestinal tract contains the highest concentration of immune cells that communicate with the microbial community, triggering the release of metabolites or immune responses, which affect the immune system directly. The gut microbiome has been shown to have a profound effect on bone quantity, quality, and overall strength in many clinical studies. Citation1 However, osteoporosis is often effectively untreated owing to the cost and side effects of approved drugs, which underscores the urgent need to develop inexpensive and safe interventions. Although the incidence of fractures varies greatly from country to country, women over 50 years of age have an average risk of up to 50%. With the aging population, the frequency of osteoporosis is increasing, which usually decreases bone strength, mass, and density and increases fragility, often leading to fractures. Dominant intestinal flora showed significant differences in composition LGG treatment regulated the various genera that were imbalanced in OVX, along with modifying those that did not change significantly in other groups with respect to the intestinal barrier, inflammation development, and bile acid metabolism. Importantly, 16S rRNA sequencing showed a significant increase in the Firmicutes/Bacteroidetes ratio during estrogen deficiency. Regarding the intestinal barrier, we found that LGG treatment ameliorated estrogen deficiency-induced inflammation and mucosal damage and increased the expression of GLP-2 R and tight junction proteins. TNF-α and IL-17 expression in colon and bone marrow increased, while TGF-β and IL-10 expression decreased however, LGG treatment modulated these changes and improved the Th17/Treg balance significantly. ![]() ![]() Th17 cells were imbalanced with Treg cells in mediastinal lymph nodes and bone marrow, with RORγt and FOXP3 expression following a similar trend. LGG was more advantageous in promoting osteogenesis, which may be responsible for the alleviation of osteoporosis. We found a protective effect of LGG treatment in OVX rats through changes in bone microarchitecture, bone biomechanics, and CTX-I, PINP, Ca, and RANKL expression levels. ![]()
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