Mast cell activation is involved in stress‐induced epithelial barrier dysfunction in the esophagus

Zhong, Chan Juan; Wang, Kun; Zhang, Lu; Yang, Chang; Zhang, Kuo; Shu, Zhao; Duan, Lingxun

doi:10.1111/1751-2980.12226

Cited by 12 publications

(13 citation statements)

References 38 publications

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“…Meanwhile, levels of CRF, the key stress hormone, raised in serum and intestinal tissues under stress. CRF mainly expresses in the central nervous system, but also can be released locally by enterochromaffin cells, immune cells, regional sensory and sympathetic nerves in peripheral tissues 15–18 . Central and peripheral administration of exogenous CRF have been shown to mimic the stress-incuced intestinal dysfunctions including increasing ion and water secretion, mucus release and epithelial permeability 17 .…”

Section: Discussionmentioning

confidence: 99%

“…These findings are in line with previous evidences that PAR2 participated in the intestinal mucosal inflammation 31 . Tryptase may directly acted on the epithelial PAR2 and rearranged the tight junction proteins and perijunctional F-actin and eventually resulted in paracellular leakage and inflammation of the gut 18 . PAR2 activation may also promote the release of pro-inflammatory peptides such as calcitonin gene-related peptide and substance P, and lead to secretion of TNFα and IFNγ which in turn increase paracellular peameability and trigger intestinal inflammation 2, 18 .…”

Section: Discussionmentioning

confidence: 99%

“…Tryptase may directly acted on the epithelial PAR2 and rearranged the tight junction proteins and perijunctional F-actin and eventually resulted in paracellular leakage and inflammation of the gut 18 . PAR2 activation may also promote the release of pro-inflammatory peptides such as calcitonin gene-related peptide and substance P, and lead to secretion of TNFα and IFNγ which in turn increase paracellular peameability and trigger intestinal inflammation 2, 18 . Then we tend to believe that elevated MCs and PAR2 signaling may also play a significant role in the FAE hyper-permeability under stress conditions.…”

Section: Discussionmentioning

confidence: 99%

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Stress induces more serious barrier dysfunction in follicle-associated epithelium than villus epithelium involving mast cells and protease-activated receptor-2

Song

Bai

Qian

et al. 2017

Sci Rep

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Psychological stress has been associated with intestinal epithelial hyperpermeability, the basic process in various functional and organic bowel diseases. In the present study, we aimed to clarify the differences and underlining mechanisms in stress-induced barrier disruption in functionally and structurally distinct epitheliums, including the villus epithelium (VE) and follicle-associated epithelium (FAE), a specialized epithelium overlaid the domes of Peyer’s lymphoid follicles. Employing an Ussing Chamber system, the epithelial permeability was assessed in rats following water avoidance stress (WAS) in vivo and in mucosa tissues exposed to corticotropin-releasing factor (CRF) ex vivo. Decreased transepithelial resistance (TER) and increased paracellular and transcellular macromolecular permeability in colon, ileal VE and FAE had been observed in WAS rats and in CRF-exposed mucosa. Especially, the barrier dysfunction was more serious in the FAE. Moreover, WAS upregulated the expression of mast cell tryptase and protease-activated receptor-2 (PAR2), which positively correlated with epithelial conductance. Mast cell stabilizer cromolyn sodium obviously alleviated the barrier disruption induced by WAS in vivo and CRF in vitro. Serine protease inhibitor aprotinin and FUT-175, and selective PAR2 antagonist ENMD-1068 effectively inhibited the CRF-induced FAE hyperpermeability. Altogether, it concluded that the FAE was more susceptible to stress, and the mast cells and PAR2 signaling played crucial roles in this process.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Stress induces more serious barrier dysfunction in follicle-associated epithelium than villus epithelium involving mast cells and protease-activated receptor-2

Song

Bai

Qian

et al. 2017

Sci Rep

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“…The number of immune cells per field was thus calculated. Moreover, the number of mast cells stained with alcian blue pH 2.5 and counterstained with nuclear fast red [24] was counted in 10 fields at 100x.…”

Section: Immune Cells Countingmentioning

confidence: 99%

Hypothyroidism Induces a Moderate Steatohepatitis Accompanied by Liver Regeneration, Mast Cells Infiltration, and Changes in the Expression of the Farnesoid X Receptor

Rodríguez-Castelán

Corona-Pérez

Nicolás-Toledo

et al. 2016

Exp Clin Endocrinol Diabetes

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Hypothyroidism is associated with the development of non-alcoholic steatohepatitis, but cellular mechanisms have been scarcely analyzed. Thyroid hormones regulate the synthesis and secretion of bile acids that are endogenous ligands of the farnesoid receptor (FXRα), which have been involved in the development of non-alcoholic steatohepatitis. However, the relationship between thyroid hormones and FXRα expression in the liver is yet unknown. Control (=6) and methimazole-induced hypothyroid (=6) female rabbits were used to evaluate the amount of lipids and glycogen, vascularization, hepatocytes proliferation, immune cells infiltration, and expression of FXRα. Student- or Mann-Whitney tests were carried out to determine significant differences. Hypothyroidism induced steatosis, glycogen loss, fibrosis, and a minor vascularization in the liver. In contrast, hypothyroidism increased the proliferation of hepatocytes and the infiltration of mast cells, but did not modify the number of immune cells into sinusoids. These changes were associated with a minor anti-FXRα immunoreactivity of periportal hepatocytes and pericentral immune cells. Our results suggest that hypothyroidism induces a moderate non-alcoholic steatohepatitis, alllowing the hepatic regeneration. The FXRα may be involved in the development of non-alcoholic steatohepatitis in hypothyroid subjects.

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“…Eosinophils, on the other hand, are important regulators of local inflammatory response and their accumulation is linked to many inflammatory diseases [56]. Many studies have linked the damaged urothelium to activation and stimulation of the inflammatory cells in the bladder of IC/BPS patients which can trigger the release of other inflammatory mediators [57][58][59][60][61].…”

Section: Increased Inflammatory Mediatorsmentioning

confidence: 99%

Purinergic P2X7 receptors as therapeutic targets in interstitial cystitis/bladder pain syndrome; key role of ATP signaling in inflammation

Taidi

Mansfield

Bates

et al. 2019

Bladder

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Interstitial cystitis/bladder pain syndrome (IC/BPS) is a chronic lower urinary tract condition. Patients with IC/BPS suffer from debilitating pain and urinary urgency. The underlying etiology of IC/BPS is unknown and as such current treatments are mostly symptomatic with no real cure. Many theories have been proposed to describe the etiology of IC/BPS, but this review focuses on the role of inflammation. In IC/BPS patients, the permeability of the urothelium barrier is compromised and inflammatory cells infiltrate the bladder wall. There are increased levels of many inflammatory mediators in patients with IC/BPS and symptoms such as pain and urgency that have been associated with the degree of inflammation. Recent evidence has highlighted the role of purinergic receptors, specifically the P2X7 receptor, in the process of inflammation. The results from studies in animals including cyclophosphamide-induced hemorrhagic cystitis strongly support the role of P2X7 receptors in inflammation. Furthermore, the deletion of the P2X7 receptor or antagonism of this receptor significantly reduces inflammatory mediator release from the bladder and improves symptoms. Research results from IC/BPS patients and animal models of IC/BPS strongly support the crucial role of inflammation in the pathophysiology of this painful disease. Purinergic signaling and purinergic receptors, especially the P2X7 receptor, play an undisputed role in inflammation. Purinergic receptor antagonists show positive results in treating different symptoms of IC/BPS.

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Mast cell activation is involved in stress‐induced epithelial barrier dysfunction in the esophagus

Cited by 12 publications

References 38 publications

Stress induces more serious barrier dysfunction in follicle-associated epithelium than villus epithelium involving mast cells and protease-activated receptor-2

Stress induces more serious barrier dysfunction in follicle-associated epithelium than villus epithelium involving mast cells and protease-activated receptor-2

Hypothyroidism Induces a Moderate Steatohepatitis Accompanied by Liver Regeneration, Mast Cells Infiltration, and Changes in the Expression of the Farnesoid X Receptor

Purinergic P2X7 receptors as therapeutic targets in interstitial cystitis/bladder pain syndrome; key role of ATP signaling in inflammation

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