How Stress Induces Intestinal Hypersensitivity

Buret, André G.

doi:10.2353/ajpath.2006.050958

Cited by 27 publications

(9 citation statements)

References 28 publications

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“…The intestinal lining also harbors immune cells, including dendritic cells and T cells (Coombes and Powrie, 2008, Fagarasan et al, 2010), and may serve as a source of circulating cytokines. Increased exposure to toxins, food allergens, and stress may promote a loss of protective microorganisms and increase inflammation in the gut, thus contributing to behavioral symptoms associated with increased inflammatory cytokines (Arrieta et al, 2006, Buret, 2006). Furthermore, manipulation of the gut microbiota of mice altered behavior and hippocampal brain-derived neurotrophic factor (BDNF) content independent of changes in circulating inflammatory cytokines and neuroendocrine hormones, indicating a potentially direct gut to brain connection that can influence behavior (Bercik et al, 2011).…”

Section: Cytokines and Depressionmentioning

confidence: 99%

Inflammatory cytokines in depression: Neurobiological mechanisms and therapeutic implications

Felger¹,

Lotrich²

2013

Neuroscience

923

609

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Mounting evidence indicates that inflammatory cytokines contribute to the development of depression in both medically ill and medically healthy individuals. Cytokines are important for development and normal brain function, and have the ability to influence neurocircuitry and neurotransmitter systems to produce behavioral alterations. Acutely, inflammatory cytokine administration or activation of the innate immune system produces adaptive behavioral responses that promote conservation of energy to combat infection or recovery from injury. However, chronic exposure to elevated inflammatory cytokines and persistent alterations in neurotransmitter systems can lead to neuropsychiatric disorders and depression. Mechanisms of cytokine behavioral effects involve activation of inflammatory signaling pathways in the brain that results in changes in monoamine, glutamate, and neuropeptide systems, and decreases in growth factors, e.g. brain derived neurotrophic factor. Furthermore, inflammatory cytokines may serve as mediators of both environmental (e.g. childhood trauma, obesity, stress, and poor sleep) and genetic (functional gene polymorphisms) factors that contribute to depression’s development. This review explores the idea that specific gene polymorphisms and neurotransmitter systems can confer protection from or vulnerability to specific symptom dimensions of cytokine-related depression. Additionally, potential therapeutic strategies that target inflammatory cytokine signaling or the consequences of cytokines on neurotransmitter systems in the brain to prevent or reverse cytokine effects on behavior are discussed.

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Section: Cytokines and Depressionmentioning

confidence: 99%

Inflammatory cytokines in depression: Neurobiological mechanisms and therapeutic implications

Felger¹,

Lotrich²

2013

Neuroscience

923

609

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“…After severe burn injury, a variety of stressors such as mental stimulation, local tissue damage, ischemia/hypoxia, inflammation, and surgical operation can enhance the activities of both hypothalamic-pituitary-adrenal axis and sympathetic nerve system, leading to severe systemic stress responses. The stress may play an important role in the intestinal barrier dysfunction and hyperpermeability in some diseases including burn injury [38, 39]. An animal experiment has demonstrated the intestinal permeability, bacterial translocation, and proinflammatory cytokines such as interferon-γ (IFN-γ) are significantly increased by stress stimulation in C57BL/6 J mice, but not in the severe combined immunodeficiency (SCID) and IFN-γ-deficient mice [40], indicating that the stress-induced intestinal barrier dysfunction depends on the presence of CD4 + T lymphocytes and IFN-γ.…”

Section: Reviewmentioning

confidence: 99%

“…Based on the reported studies, it is believed that MLCK also plays a critical role in intestinal barrier dysfunction after severe burn injury. Some previous studies have shown that MLCK is critical to intestinal epithelial barrier dysfunction, increased permeability, and the relocalization of TJPs ZO-1, occludin, and claudins induced by a number of pathophysiological conditions associated with severe burns such as stress, shock, ischemia/hypoxia, inflammation, and infection [5, 39, 47, 97, 101–104]. The previous animal studies have revealed that MLCK chemical inhibitor ML-9 or peptide inhibitor PIK could significantly alleviate the barrier dysfunction, the changes of TJPs, the increase of MLC phosphorylation, and the hyperpermeability of intestinal epithelia in mice subjected to severe burns [94, 105].…”

Section: Reviewmentioning

confidence: 99%

Intestinal barrier dysfunction in severe burn injury

Wang

et al. 2019

Burns &Amp; Trauma

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Severe burn injury is often accompanied by intestinal barrier dysfunction, which is closely associated with post-burn shock, bacterial translocation, systemic inflammatory response syndrome, hypercatabolism, sepsis, multiple organ dysfunction syndrome, and other complications. The intestinal epithelium forms a physical barrier that separates the intestinal lumen from the internal milieu, in which the tight junction plays a principal role. It has been well documented that after severe burn injury, many factors such as stress, ischemia/hypoxia, proinflammatory cytokines, and endotoxins can induce intestinal barrier dysfunction via multiple signaling pathways. Recent advances have provided new insights into the mechanisms and the therapeutic strategies of intestinal epithelial barrier dysfunction associated with severe burn injury. In this review, we will describe the current knowledge of the mechanisms involved in intestinal barrier dysfunction in response to severe burn injury and the emerging therapies for treating intestinal barrier dysfunction following severe burn injury.

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“…alteration of chromatin structure through effects on DNA methylation lead to a lasting sensitization of stress response systems following pre-natal or post-natal stress exposure [ 13 ]) could increase the risk both of developing major depression and developing allergies. In the case of food allergies, stressors may also contribute to intestinal hypersensitivity by altering transepithelial permeability, see a brief review of possible mechanisms by Buret [ 14 ]. However, there is a consensus that most self-reported food allergies in the community are not attributable to Type I or Type IV hypersensitivity [ 15 ], leading to the suspicion that there may be false positive reports based on a misinterpretation of somatic symptoms.…”

Section: Introductionmentioning

confidence: 99%