This review states that stress, through the brain-gut axis, may cause intestinal barrier dysfunction, mainly via the systemic and peripheral release of corticotropin-releasing factor. It also reports that stress and CRF increase intestinal permeability in animal models and that this enhanced permeability could lead to excessive uptake of luminal antigens and bacterial products that may initiate mucosal inflammation.

The review says that intestinal permeability is associated with translocation of bacteria or bacterial products from the gut to the bloodstream, lymph nodes, and other organs. It also notes that this effect could be mimicked by administering corticotropin-releasing hormone, linking stress signaling to barrier disruption.

This article reports that physiological and psychological stress can impair intestinal barrier function. It describes increased intestinal permeability after stress and discusses mechanisms involving tight junction regulation and downstream mucosal consequences.

The abstract describes evidence that stress increases intestinal permeability and that corticotropin-releasing factor is a key mediator of this response. It also notes that CRF-related signaling has been linked to altered epithelial barrier function in the gut.

This review states that intestinal epithelial tight junctions can be disrupted by stress through signaling pathways triggered by stress hormones such as glucocorticoids. It also reports that stress can increase intestinal permeability, remodel tight junction proteins, and promote luminal bacterial translocation to mesenteric lymph nodes in animal models.

This review states that stress can alter intestinal permeability and barrier integrity through neural, immune, and endocrine pathways. It also discusses that stress-related barrier dysfunction can permit increased passage of luminal contents across the epithelium.

This review explains that tight junctions between enterocytes are a major component of the intestinal barrier and that disruption of tight junction structure increases paracellular permeability. It provides the mechanistic basis for how barrier disruption can increase passage of luminal substances.

The study reports that corticotropin-releasing factor reduced barrier function in intestinal epithelial preparations and increased epithelial permeability. This supports a direct CRF effect on the intestinal barrier, consistent with stress-related permeability changes.

The abstract reports that stress induced intestinal barrier dysfunction and that mast cell activation participated in this response. It describes increased permeability in association with stress, providing experimental support for stress-related barrier disruption.

The intestinal barrier is formed by enterocyte membranes, tight junctions, secreted mucus, and immunologic factors. The abstract states that dysfunction of this barrier can be caused by different types of stress and can lead to increased intestinal permeability and endotoxin translocation, which can trigger local or systemic inflammatory reactions.

The authors state that "An impaired intestinal barrier function can be detrimental to the host as it may allow the translocation of luminal antigens and toxins into the subepithelial tissue and bloodstream." They summarize that "In vitro and animal studies strongly suggest that psychosocial stress is one of the factors that can increase intestinal permeability via mast-cell dependent mechanisms." They also note that chronic psychological stress in rodents "resulted in a decrease of TJ occludin and claudin-1" and that glucocorticoid receptor blockade prevented "an increase in intestinal permeability... caused by psychological stress," indicating disruption of tight junction proteins as a mechanism for stress‑induced hyperpermeability.

This review summarizes evidence that stress and corticotropin-releasing factor increase intestinal permeability and that mast cells help mediate the effect. It also links barrier dysfunction to movement of luminal antigens and microbes across the intestinal epithelium.

The study reports that psychological stress increased small intestinal permeability in healthy humans, measured by the lactulose/mannitol ratio. It also found that the mast cell stabilizer disodium cromoglycate blocked the effect of stress and CRF on permeability.

This study reports that osmotic stress disrupted tight junctions and barrier function in Caco-2 intestinal epithelial monolayers without affecting cell viability. It further states that tight junction disruption and barrier dysfunction were associated with JNK-dependent remodeling of the actin cytoskeleton, and that cold restraint stress in rat ileum caused redistribution of occludin and ZO-1 away from intercellular junctions.

The single layer of intestinal epithelial cells, connected by tight junctions (TJs), forms a physical and functional barrier between the external environment in the intestinal lumen and the internal host milieu. Increased intestinal permeability can therefore result from either loss of epithelial cells or from disruption of TJs. It is evident that heat stress and vigorous exercise increase intestinal epithelial TJ permeability and that several culprits are implicated in damage to the TJ complex, including epithelial injury, oxidation, ischemia, tissue acidosis, and mast cell activation. Stress-related barrier dysfunction is associated with an increase in permeation of luminal antigens and endotoxins into the circulation.

Deficits in intestinal permeability may underpin the chronic low-grade inflammation observed in disorders such as depression and the gut microbiome plays a critical role in regulating intestinal permeability. Tight junctions are complex protein structures that consist of transmembrane proteins such as claudin, occludin, and tricellulin, which connect with the opposing plasma membrane, forming a mechanical link between epithelial cells and establishing a barrier to paracellular diffusion. Stress has been associated with an increase in gut permeability. Corticotrophin releasing factor (CRF) and its receptors play a key role in stress-induced gut permeability dysfunction. In response to an acute stressor, colonic paracellular permeability increases. Early life stress has also been demonstrated to enhance plasma corticosterone in rat pups and is associated with an increase in intestinal permeability and bacterial translocation to the liver and spleen.

Psychosocial stress has been shown to increase intestinal permeability in both animal models and humans. Stress-induced activation of the hypothalamic–pituitary–adrenal axis and release of corticotropin-releasing hormone (CRH) can modulate epithelial tight junctions and increase paracellular permeability. Increased intestinal permeability due to stress allows increased translocation of luminal antigens and bacteria, which can activate mucosal immune responses and contribute to gastrointestinal symptoms and disease. Animal studies demonstrate that stress leads to bacterial translocation to mesenteric lymph nodes and other organs.

Exposure to acute or chronic psychological stress affects intestinal barrier function. Stress-induced activation of mast cells and the release of mediators such as CRF, cytokines, and proteases can alter tight junction structure and function, leading to increased paracellular permeability. The resulting impaired barrier function facilitates translocation of luminal antigens and bacteria to the lamina propria and beyond, thereby promoting immune activation and inflammation. Experimental models show that stress can increase bacterial translocation to mesenteric lymph nodes.

In this animal study, rats were exposed to chronic psychological stress (water avoidance). The authors report that stress led to "increased intestinal permeability" and that stressed rats developed "sensitization to luminal antigens" with enhanced mucosal immune responses after antigen challenge. They attribute these effects to stress-induced barrier dysfunction, showing that chronic stress facilitates the passage of antigens across the intestinal epithelium and promotes antigen-specific immune activation.

This study demonstrates that acute restraint stress in rats "significantly increased colonic permeability" to markers such as FITC-dextran and was associated with "increased bacterial translocation" to mesenteric lymph nodes and other tissues. The authors show that these effects were prevented by CRF receptor antagonists and mast cell stabilizers, implicating stress-mediated CRF release and mast cell activation. They conclude that stress-induced disruption of the colonic barrier allows bacteria from the lumen to cross the epithelium and reach extra-intestinal sites.

Reviewing experimental data, the authors note that chronic psychological stress "has been shown to increase intestinal permeability" and alter mucosal immune homeostasis. They describe that stress-induced changes in the epithelial barrier are linked to "disruption of tight junction complexes" and increased paracellular flux of luminal antigens. This enhanced translocation of antigens into the lamina propria is reported to drive mucosal immune activation and inflammation, demonstrating a mechanistic link between stress, tight junction disruption, and antigen passage.

This experimental paper shows that acute stress increased intestinal permeability to macromolecules and that this was associated with alterations in epithelial tight junctions. Electron microscopy and morphometric analyses indicated structural changes at the level of tight junctions between enterocytes after stress exposure. The authors conclude that stress-induced impairment of the barrier "facilitates the passage of luminal antigens" across the intestinal epithelium, which can then interact with the mucosal immune system.

In this human study, public speaking stress was used as a psychosocial stressor. The authors report that in male subjects with high cortisol responses, "colonic paracellular permeability was significantly increased" after the stressor compared with control conditions. They interpret this as evidence that acute psychological stress can increase intestinal permeability in humans, particularly in those with strong HPA axis activation, providing a pathway for increased exposure of the mucosal immune system to luminal contents.

Psychological stress has been shown to increase intestinal permeability, possibly through mechanisms involving alterations in tight junction proteins and stress hormone signaling. Increased permeability of the intestinal barrier may allow translocation of microbial products into the systemic circulation, stimulating inflammatory responses. Several studies in animals indicate that stress results in bacterial translocation from the gut lumen to mesenteric lymph nodes and other extra-intestinal sites. These findings support a link between stress-induced barrier disruption and increased passage of luminal bacteria and antigens.

This review notes that "stress may affect different physiologic functions of the gastrointestinal tract including... mucosal permeability and barrier function" and lists as a major effect of stress "increase in intestinal permeability." It further explains that corticotropin-releasing factor (CRF) has potent effects on the gut including "increase of gut permeability" and that mast cells translate stress signals into mediators that "may profoundly affect the gastrointestinal physiology." The article discusses that increased permeability under stress can contribute to food antigen-related adverse responses and other gut disorders, consistent with enhanced passage of luminal antigens across a compromised epithelial barrier.

Discussing mechanisms, the authors describe that stress-induced activation of CRF receptors and mast cells leads to "changes in epithelial tight junctions" and increased intestinal permeability. They note that disruption of tight junction integrity under stress conditions "permits the passage of luminal antigens and bacteria" into the lamina propria, where they can activate mucosal immune responses. The review links these changes to the development or exacerbation of conditions such as IBS, IBD and food allergies, emphasizing the role of stress in compromising tight junctions between enterocytes.

In this study, the effect of acute psychological stress on small intestinal permeability was examined in healthy volunteers using a public speaking paradigm. Small intestinal permeability, assessed by urinary excretion of orally administered sugars, was significantly increased during stress in subjects who showed a marked cortisol response. The authors concluded that acute psychological stress can increase small intestinal permeability in humans, potentially via cortisol-mediated effects on intestinal epithelial tight junctions.

Chronic psychological stress induced by repeated water-avoidance stress resulted in increased colonic permeability in mice, as assessed by transepithelial flux of fluorescein isothiocyanate–dextran. This was accompanied by disruption and redistribution of tight junction proteins, including occludin and ZO-1, in colonic epithelial cells. The stressed mice also exhibited increased bacterial translocation to mesenteric lymph nodes and elevated mucosal inflammatory markers. The study links chronic stress to tight junction dysregulation, barrier dysfunction, and increased translocation of luminal bacteria.

Maternal separation as a model of early life stress significantly enhanced plasma corticosterone levels in rat pups and was associated with increased intestinal permeability, as measured by translocation of macromolecules across the gut epithelium. Early life stress led to increased bacterial translocation to the liver and spleen. These findings suggest that stress-induced changes in intestinal barrier function facilitate the passage of luminal bacteria and antigens into extra-intestinal sites, potentially through effects on epithelial tight junctions.

Physiologic stress has been reported to alter intestinal permeability through tight junction regulation in multiple experimental models. Commonly proposed mechanisms include stress-hormone signaling, myosin light chain kinase activation, and cytoskeletal remodeling that redistribute tight-junction proteins such as occludin and ZO-1.