The gut epithelium is a polarized monolayer that exhibits apical and basolateral membrane surfaces. Monolayer cell components are joined side by side via protein complexes known as tight junction proteins (TJPs), expressed at the most apical extreme of the basolateral membrane. The gut epithelium is a physical barrier that determinates intestinal permeability, referred to as the measurement of the transit of molecules from the intestinal lumen to the bloodstream or, conversely, from the blood to the gut lumen. TJPs play a role in the control of intestinal permeability that can be disrupted by stress through signal pathways triggered by the ligation of receptors with stress hormones like glucocorticoids. Preclinical studies conducted under in vitro and/or in vivo conditions have addressed underlying mechanisms that account for the impact of stress on gut permeability. These mechanisms may provide insights for novel therapeutic interventions in diseases in which stress is a risk factor, like irritable bowel syndrome. The focus of this study was to review, in an integrative context, the neuroendocrine effects of stress, with special emphasis on TJPs along with intestinal permeability.

The intestinal epithelial barrier regulates paracellular transport, and its dysfunction is associated with inflammatory and metabolic diseases. Among dietary fibers, inulin has attracted considerable attention due to its beneficial effects on intestinal health. Inulin’s actions have been attributed to protecting the structure and function of gut barrier components against inflammatory-associated damage. This review integrates preclinical and clinical studies evaluating the impact of inulin on intestinal permeability. Evidence from in vitro and in vivo models shows that inulin regulates the expression of tight junction proteins (TJPs), Paneth cell proliferation, and antimicrobial peptides, and modulates inflammatory signaling pathways. In addition, inulin prebiotic activity, via microbiota, stimulates the production of short-chain fatty acids (SCFAs) as butyrate that reinforces the barrier function. Understanding these pathways highlights the therapeutic potential of inulin as a nutritional strategy for treating barrier dysfunction. Clinical studies in obesity, metabolic disorders and inflammatory intestinal disease have associated inulin supplementation with improvements in biomarkers of intestinal permeability. Future studies are needed to test inulin’s safety in order to prevent potential risks and hazards.