Chronic stress induces mast cell–dependent bacterial adherence and initiates mucosal inflammation in rat intestine

Söderholm, Johan D.; Yang, Ping‐Chang; Ceponis, Peter J. M.; Vohra, Angeli; Riddell, Robert H.; Sherman, Philip M.; Perdue, Mary H.

doi:10.1053/gast.2002.36019

Cited by 315 publications

(313 citation statements)

References 34 publications

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“…In two recent studies (29,33), our laboratory found that rats exposed to chronic stress develop a prolonged barrier defect to macromolecules and epithelial mitochondrial damage (29). Longer exposure to stress induces bacterial internalization into the epithelium and inflammatory cell infiltration in the lamina propria, suggesting that stress can be important in the initiation of intestinal inflammation (33).…”

Section: Discussionmentioning

confidence: 99%

Neonatal maternal separation predisposes adult rats to colonic barrier dysfunction in response to mild stress

Söderholm¹,

Yates²,

Gareau³

et al. 2002

American Journal of Physiology-Gastrointestinal and Liver Physi

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207

206

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. Neonatal maternal separation predisposes adult rats to colonic barrier dysfunction in response to mild stress. Am J Physiol Gastrointest Liver Physiol 283: G1257-G1263, 2002. First published August 28, 2002 10.1152/ajpgi.00314.2002Intestinal dysfunction is related to stress and early life events, but the mechanisms are largely unknown. Our aim was to determine whether early trauma predisposes adult rats to intestinal mucosal dysfunction in response to stress. Neonatal Sprague-Dawley rats were individually separated from their mothers for 3 h/day at 4-21 days of age. Between days 80 and 90, separated and control rats were subjected to mild acute stress (30-min water avoidance) or sham stress. Mucosal barrier function and ion transport were assessed in colonic tissues mounted in Ussing chambers. Mild stress increased short-circuit current, conductance, and transepithelial transport of macromolecules in separated rats, while having minimal effects in controls. Pretreatment of the separated rats with a corticotropin-releasing hormone (CRH) antagonist, the peptide ␣-helical CRH(9-41) injected intraperitoneally 20 min before stress, abolished the stress-induced mucosal changes. Our results indicate that neonatal trauma can induce phenotypic changes in adulthood, including enhanced vulnerability of the gut mucosa to stress via mechanisms involving peripherally located CRH receptors.behavior; corticotropin-releasing hormone; electron microscopy; ion transport; intestinal permeability HUMANS EXPERIENCE STRESS OF various types during daily life, and adequate responses to these stressors are necessary for survival. If the severity or the chronicity of the stressful experience exceeds the adaptive capacity, the individual will be predisposed to illness and disease in multiple organ systems (21). A large number of studies have shown that early-life experience plays an important role in stress responsiveness throughout life (8). In animal models, neonatal adversity can result in permanent functional changes in the stress-mediating systems of the central nervous system (15). For example, newborn rats subjected to maternal separation demonstrate increased release of corticotropinreleasing hormone (CRH), altered expression of glucocorticoid receptors, as well as changes in the norepinephrine and GABA systems (3, 4). Recently, it was also shown in humans that adverse early-life events are associated with hyperresponsiveness to stress and alterations in the hypothalamic-pituitaryadrenal (HPA) axis (10).There is evidence that early-life trauma and ongoing psychological stress can affect the clinical course of intestinal disorders (16,17,20,26) and also reactivate inflammation in experimental colitis (6,9,22,25). The mechanisms underlying stress-induced exacerbations of intestinal diseases are, however, largely unknown. One possible link between intestinal disease and stress is a change in mucosal function. Our previous studies have shown that acute stress in rats induces enhanced intestinal epithelial permeability to macromolecu...

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Section: Discussionmentioning

confidence: 99%

Neonatal maternal separation predisposes adult rats to colonic barrier dysfunction in response to mild stress

Söderholm¹,

Yates²,

Gareau³

et al. 2002

American Journal of Physiology-Gastrointestinal and Liver Physi

Self Cite

207

206

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“…70 Notably, the MC-mediated mucosal barrier dysfunction may also be blamed, because the epithelial function and morphology were unchanged and no inflammatory cell infiltration was observed in MC-deficient rats by chronic stress. 71 On the other hand, MCs have also been documented to have a protective role in colonic colitis, since deletion of MCs in IL-10-deficient mice resulted in enhanced T helper 1 type (Th1) pro-inflammatory cytokines and inflammatory signaling. 72 It was concluded that MCs may suppress Th1 immune response and inflammation.…”

Section: Mast Cells In Gut Immunomodulation and Inflammationmentioning

confidence: 99%

Mast Cells and Irritable Bowel Syndrome: From the Bench to the Bedside

Zhang

Song

Hou

2016

J Neurogastroenterol Motil

107

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Irritable bowel syndrome (IBS) is traditionally defined as a functional disorder since it lacks demonstrable pathological abnormalities. However, in recent years, low grade inflammatory infiltration, often rich in mast cells, in both the small and large bowel, has been observed in some patients with IBS. The close association of mast cells with major intestinal functions, such as epithelial secretion and permeability, neuroimmune interactions, visceral sensation, and peristalsis, makes researchers and gastroenterologists to focus attention on the key roles of mast cells in the pathogenesis of IBS. Numerous studies have been carried out to identify the mechanisms in the development, infiltration, activation, and degranulation of intestinal mast cells, as well as the actions of mast cells in the processes of mucosal barrier disruption, mucosal immune dysregulation, visceral hypersensitivity, dysmotility, and local and central stress in IBS. Moreover, therapies targeting mast cells, such as mast cell stabilizers (cromoglycate and ketotifen) and antagonists of histamine and serotonin receptors, have been tried in IBS patients, and have partially exhibited considerable efficacy. This review focuses on recent advances in the role of mast cells in IBS, with particular emphasis on bridging experimental data with clinical therapeutics for IBS patients.

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“…17,18 Previous observations by the same group of investigators found that chronic psychological stress induced mast cell-dependent bacterial attachment to the epithelium and increased bacterial translocation. 19 The present findings by Yang and colleagues 5 underscore the need for more research into how inadequate responses to bacteria that favor the development of allergy may be modulated by stress.…”

mentioning

confidence: 68%

How Stress Induces Intestinal Hypersensitivity

Buret

2006

The American Journal of Pathology

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Chronic stress induces mast cell–dependent bacterial adherence and initiates mucosal inflammation in rat intestine

Cited by 315 publications

References 34 publications

Neonatal maternal separation predisposes adult rats to colonic barrier dysfunction in response to mild stress

Neonatal maternal separation predisposes adult rats to colonic barrier dysfunction in response to mild stress

Mast Cells and Irritable Bowel Syndrome: From the Bench to the Bedside

How Stress Induces Intestinal Hypersensitivity

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