Full thickness eosinophilia in oesophageal leiomyomatosis and idiopathic eosinophilic oesophagitis. A common allergic inflammatory profile?

Nicholson, Andrew G.; Li, Dechun; Pastorino, Ugo; Goldstraw, Peter; Jeffery, Peter K.

doi:10.1002/(sici)1096-9896(199710)183:2<233::aid-path936>3.0.co;2-z

Cited by 51 publications

(29 citation statements)

References 24 publications

(24 reference statements)

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“…Thus, there is a differential requirement of IL-5 in regulating esophageal and intestinal eosinophilia. A clinical study has demonstrated elevated levels of IL-4-secreting T cells in esophageal lesions of patients with secondary eosinophilic esophagitis, supporting a central role of Th2 cell responses in the pathogenesis of eosinophilic esophagitis (34). The identification of a Th2-associated cytokine with the immunopathogenesis of eosinophilic esophagitis suggests that drugs used to treat allergy may also be useful for eosinophilic esophageal disorders.…”

Section: Discussionmentioning

confidence: 94%

IL-5 Promotes Eosinophil Trafficking to the Esophagus

Mishra

Hogan

Brandt

et al. 2002

The Journal of Immunology

315

250

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Eosinophil infiltration into the esophagus occurs in a wide range of diseases; however, the underlying pathophysiological mechanisms involved are largely unknown. We now report that the Th2 cytokine, IL-5, is necessary and sufficient for the induction of eosinophil trafficking to the esophagus. We show that transgenic mice overexpressing IL-5 under the control of a T cell (CD2) or a small intestinal enterocyte (fatty acid-binding protein) promoter have markedly increased eosinophil numbers in the esophagus. For example, esophageal eosinophil levels are 1.9 ± 0.9 and 121 ± 14 eosinophils/mm2 in wild-type and CD2-IL-5-transgenic mice, respectively. Consistent with this effect being mediated by a systemic mechanism, pharmacological administration of IL-5 via a miniosmotic pump in the peritoneal cavity resulted in blood and esophageal eosinophilia. To examine the role of IL-5 in oral Ag-induced esophageal eosinophilia, eosinophilic esophagitis was induced by allergen exposure in IL-5-deficient and wild-type mice. Importantly, IL-5-deficient mice were resistant to eosinophilic esophagitis. Finally, we examined the role of eotaxin when IL-5 was overproduced in vivo. Esophageal eosinophil levels in CD2-IL-5-transgenic mice were found to decrease 15-fold in the absence of the eotaxin gene; however, esophageal eosinophil numbers in eotaxin-deficient IL-5-transgenic mice still remained higher than wild-type mice. In conclusion, these studies demonstrate a central role for IL-5 in inducing eosinophil trafficking to the esophagus.

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Section: Discussionmentioning

confidence: 94%

IL-5 Promotes Eosinophil Trafficking to the Esophagus

Mishra

Hogan

Brandt

et al. 2002

The Journal of Immunology

315

250

View full text Add to dashboard Cite

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“…17,[53][54][55][56][57] In addition, autopsy reports find increased levels of mast cells through the full thickness of the esophagus. 58 Unlike eosinophil-deficient mice, mast cell-deficient mice are not protected from strictures. 51 They do, however, have decreased smooth muscle proliferation, as well as decreased dysmotility, indicating that mast cells affect esophageal motor function.…”

Section: Innate Immune Cellsmentioning

confidence: 99%

Eosinophilic Esophagitis

Aceves¹

2015

Immunology and Allergy Clinics of North America

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Eosinophilic esophagitis (EoE) is a clinicopathologic disease of increasing prevalence. Because EoE is a chronic disease, its prevalence will continue to increase. Antigen triggers, including food and aeroallergens, drive eosinophilic and T helper cell type 2 inflammation, resulting in subepithelial fibrosis; this esophageal remodeling is the likely underlying pathogenesis for complications of narrowing, rigidity, and food impactions. Management includes dietary antigen elimination and topical corticosteroids. Long-term therapy and repeated endoscopy are often needed; consideration must be given to maintenance regimens and side effects. This review describes the clinical features, treatment options, epidemiology, and pathogenesis of EoE.

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“…Studies of esophageal biopsy specimens from patients with EoE have revealed mast cells in the epithelium, lamina propria, and muscularis mucosae (1,5,142). A report of a patient with idiopathic eosinophilic esophagitis who had an esophagectomy described mast cells in the muscularis propria as well (111).…”

Section: Eosinophils and Mast Cellsmentioning

confidence: 99%

Tissue remodeling in eosinophilic esophagitis

Cheng¹,

Souza

Spechler

2012

American Journal of Physiology-Gastrointestinal and Liver Physi

109

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Eosinophilic esophagitis (EoE) is a recently recognized, immune-mediated disease characterized clinically by symptoms of esophageal dysfunction and histologically by eosinophil-predominant inflammation. The chronic esophageal eosinophilia of EoE is associated with tissue remodeling that includes epithelial hyperplasia, subepithelial fibrosis, and hypertrophy of esophageal smooth muscle. This remodeling causes the esophageal rings and strictures that frequently complicate EoE and underlies the mucosal fragility that predisposes to painful mucosal tears in the EoE esophagus. The pathogenesis of tissue remodeling in EoE is not completely understood, but emerging studies suggest that secretory products of eosinophils and mast cells, as well as cytokines produced by other inflammatory cells, epithelial cells, and stromal cells in the esophagus, all contribute to the process. Interleukin (IL)-4 and IL-13, Th2 cytokines overproduced in allergic disorders, have direct profibrotic and remodeling effects in EoE. The EoE esophagus exhibits increased expression of transforming growth factor (TGF)-β1, which is a potent activator of fibroblasts and a strong inducer of epithelial-mesenchymal transition. In addition, IL-4, IL-13, and TGF-β all have a role in regulating periostin, an extracellular matrix protein that might influence remodeling by acting as a ligand for integrins, by its effects on eosinophils or by activating fibrogenic genes in the esophagus. Presently, few treatments have been shown to affect the tissue remodeling that causes EoE complications. This report reviews the potential roles of fibroblasts, eosinophils, mast cells, and profibrotic cytokines in esophageal remodeling in EoE and identifies potential targets for future therapies that might prevent EoE complications.

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Full thickness eosinophilia in oesophageal leiomyomatosis and idiopathic eosinophilic oesophagitis. A common allergic inflammatory profile?

Cited by 51 publications

References 24 publications

IL-5 Promotes Eosinophil Trafficking to the Esophagus

IL-5 Promotes Eosinophil Trafficking to the Esophagus

Eosinophilic Esophagitis

Tissue remodeling in eosinophilic esophagitis

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