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The intestinal microbiota and gut barrier function constitute a dynamic physiological system critical for maintaining host health and homeostasis [1, 11]. The gut microbiota is a vast community of microorganisms that performs essential roles in nutrient metabolism, the production of short-chain fatty acids (SCFAs), and the maturation of the host immune system [7, 17]. Complementing this, the gut barrier acts as a selective physical and chemical interface, primarily composed of a mucus layer and a single layer of epithelial cells joined by tight junction proteins like zonula occludens-1 and occludin [1, 5]. This system prevents the translocation of pathogens and pro-inflammatory molecules, such as lipopolysaccharides (LPS), into the systemic circulation [5, 10]. Dysregulation of this interplay, often referred to as "leaky gut" or increased intestinal permeability, is a hallmark of numerous conditions, including inflammatory bowel disease (IBD), metabolic syndrome, and certain neurodegenerative disorders [2, 11, 17]. Therapeutic interventions, such as probiotics, prebiotics, and fecal microbiota transplants, aim to restore microbial diversity and strengthen barrier integrity to mitigate systemic inflammation and disease progression [7, 9, 14]. Pharmacological agents like larazotide acetate and rifaximin are also employed to specifically target barrier permeability and microbial overgrowth, respectively [1, 9]. Understanding the bidirectional communication between the microbiota and the host barrier is essential for developing precision medicine approaches for gastrointestinal and systemic diseases [14, 16].
Modulation of microbial composition, enhancement of tight junction protein expression, reduction of pro-inflammatory cytokines, and detoxification of lipopolysaccharides.
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