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Basic pathogenesis of eosinophilic esophagitis.

ABSTRACT: Eosinophilic esophagitis (EE) is a newly recognized disease, which has largely been called idiopathic EE, emphasizing the poor understanding of its pathogenesis. EE is a severe disease of the esophagus characterized by an accumulation of eosinophils in the esophageal mucosa, and is highly associated with atopic disease. Nevertheless, the nomenclature "eosinophilic esophagitis" describes only the tip of the iceberg of a complex disorder, as the pathogenesis of EE involves multiple tissues, cell types, and genes, and derives from complex genetic and environmental factors. This article defines the fundamental knowledge available to date that characterizes the mechanisms by which certain etiological factors cause EE, reviewing human studies, murine models, and recent knowledge regarding the involvement of environmental, cellular, molecular, and genetic factors in the development of EE.

SUBMITTER: Blanchard C

PROVIDER: S-EPMC2194642 | biostudies-literature | 2008 Jan

REPOSITORIES: biostudies-literature

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Basic pathogenesis of eosinophilic esophagitis.

Blanchard Carine C Rothenberg Marc E ME

Gastrointestinal endoscopy clinics of North America 20080101 1

Eosinophilic esophagitis (EE) is a newly recognized disease, which has largely been called idiopathic EE, emphasizing the poor understanding of its pathogenesis. EE is a severe disease of the esophagus characterized by an accumulation of eosinophils in the esophageal mucosa, and is highly associated with atopic disease. Nevertheless, the nomenclature "eosinophilic esophagitis" describes only the tip of the iceberg of a complex disorder, as the pathogenesis of EE involves multiple tissues, cell t ...[more]

PMID: 18061107

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Translating new developments in eosinophilic esophagitis pathogenesis into clinical practice.

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Eosinophilic esophagitis.

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| S-EPMC4332835 | biostudies-literature

Pathogenesis of Eosinophilic Esophagitis: A Comprehensive Review of the Genetic and Molecular Aspects.

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Project description:Eosinophilic esophagitis (EoE) is a chronic inflammatory disorder of the esophagus that is compounded by both genetic predisposition and aberrant responses to environmental antigens, particularly those that are food derived. Data have indicated a unique transcriptional response in vivo that defines EoE and that appears to be partially attributable to the T(H)2 cytokine IL-13. Moreover, a number of genetic risk variants in proinflammatory and epithelial cell genes associate with EoE susceptibility, demonstrating novel heritable mechanisms that contribute to disease risk. Here we discuss recent advances in our understanding of the intrinsic (genetic) and extrinsic (environmental) components that illustrate the complex nature of EoE.

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Role of genetics, environment, and their interactions in the pathogenesis of eosinophilic esophagitis.

Project description:The rise in incidence and prevalence of eosinophilic esophagitis (EoE) since the 1990s has prompted investigations into its pathogenesis, natural history, and management. Identified genetic variants in FLG, DSG1, CAPN14, SPINK5, and SPINK7 link EoE to epithelial barrier dysfunction, whereas variants in CCL26, POSTN, and TSLP associate EoE with T helper type 2-mediated immunity. Early-life, infectious, and geographic factors have been implicated in promoting esophageal microbial dysbiosis and, subsequently, T helper type 2 immune responses. However, research into environmental factors and their interactions with genetic variants are not as developed as their genetic counterparts. Further research into the subgroups and epigenetics of EoE will likely promote further understanding.

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| S-EPMC5787048 | biostudies-literature

Eosinophilic Esophagitis: A Review.

Project description:ImportanceEosinophilic esophagitis (EoE) is a chronic immune-mediated inflammatory disease of the esophagus that affects an estimated 34.4/100 000 people in Europe and North America. EoE affects both children and adults, and causes dysphagia, food impaction of the esophagus, and esophageal strictures.ObservationsEoE is defined by symptoms of esophageal dysfunction, such as vomiting, dysphagia, or feeding difficulties, in a patient with an esophageal biopsy demonstrating at least 15 eosinophils per high-power field in the absence of other conditions associated with esophageal eosinophilia such as gastroesophageal reflux disease or achalasia. Genetic factors and environmental factors, such as exposure to antibiotics early in life, are associated with EoE. Current therapies include proton pump inhibitors; topical steroid preparations, such as fluticasone and budesonide; dietary therapy with amino acid formula or empirical food elimination; and endoscopic dilation. In a systematic review of observational studies that included 1051 patients with EoE, proton pump inhibitor therapy was associated with a histologic response, defined as less than 15 eosinophils per high-power field on endoscopic biopsy, in 41.7% of patients, while placebo was associated with a 13.3% response rate. In a systematic review of 8 randomized trials of 437 patients with EoE, topical corticosteroid treatment was associated with histologic remission in 64.9% of patients compared with 13.3% for placebo. Patients with esophageal narrowing may require dilation. Objective assessment of therapeutic response typically requires endoscopy with biopsy.Conclusions and relevanceEoE has a prevalence of approximately 34.4/100 000 worldwide. Treatments consist of proton pump inhibitors, topical steroids, elemental diet, and empirical food elimination, with esophageal dilation reserved for patients with symptomatic esophageal narrowing.

| S-EPMC9045493 | biostudies-literature

Interleukin-15 expression is increased in human eosinophilic esophagitis and mediates pathogenesis in mice.

Project description:Background & aimsQuantitative microarray analyses have shown increased expression of interleukin-15 (IL-15) messenger RNA in the esophagus of patients with eosinophilic esophagitis (EoE), a recently recognized allergic disorder with poorly understood pathogenesis.MethodsQuantitative polymerase chain reaction and enzyme-linked immunosorbent assay analyses were performed to examine protein and transcript levels in tissue samples from patients with EoE. Tissues from IL-15Ra-deficient and wild-type (control) mice were also examined. Tissue eosinophilia was determined by immunostaining for major basic protein and flow cytometry for cell-surface receptors.ResultsQuantitative polymerase chain reaction analyses showed that levels of IL-15 and its receptor IL-15Ra were increased approximately 6- and approximately 10-fold, respectively, in tissues from patients with EoE and approximately 3- and approximately 4-fold, respectively, in mice with allergen-induced EoE. A >2-fold increase in serum IL-15 protein levels was also detected in human EoE samples compared with those from healthy individuals. Human IL-15 messenger RNA levels correlated with esophageal eosinophilia (P < .001). IL-15Ra-deficient mice were protected from allergen-induced esophageal eosinophilia compared with controls (P < .001), even though similar levels of airway eosinophilia were observed in all mice. IL-15 activated STAT5 and CD4(+) T cells to produce cytokines that act on eosinophils. Incubation of primary esophageal epithelial cells from mice and humans with IL-15 caused a dose-dependent increase in the mRNA expression and protein levels of eotaxin-1, -2, and -3.ConclusionsIL-15 mediates in the pathogenesis of EoE. IL-15 activates CD4(+) T cells to produce cytokines that act on eosinophils.

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MicroRNA assays of eosinophilic esophagitis

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-09-01 | E-GEOD-55795 | biostudies-arrayexpress

Recent advances in eosinophilic esophagitis.

Project description:Eosinophilic esophagitis is a chronic, antigen-driven, eosinophil-predominant inflammatory disease of the esophagus and affects both children and adults. Cutting-edge technologies, such as genome-wide association studies, have advanced our understanding of the disease pathogenesis at a remarkable rate. Recent insights from genetic and mechanistic studies have concluded that a complex interplay between genetic and environmental risk factors, allergic sensitization, and esophageal-specific pathways leads to disease pathogenesis. Importantly, recent epidemiologic studies have found that the incidence and prevalence of eosinophilic esophagitis continue to rise. New guidelines have advocated the elimination of the term proton pump inhibitor (PPI)-responsive esophageal eosinophilia and have recommended using PPIs as a first-line treatment modality. Systemic reviews and meta-analyses confirm the efficacy of PPIs, topical corticosteroids, and empiric food elimination diets. Unmet needs include the development of birth cohort studies, validated diagnostic scoring systems, minimally invasive disease-monitoring methods, and the development of new therapies.

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