Antigen inhalation induces mast cells and eosinophils infiltration in the guinea pig esophageal epithelium involving histamine-mediated pathway

Yu, Shaoyong; Stahl, E. A.; Li, Qing; Ouyang, Ann

doi:10.1016/j.lfs.2007.12.002

Cited by 34 publications

(41 citation statements)

References 39 publications

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“…This may include histamine, generated from mast cells or basophils, as thioperamide, a non-selective blocker of the histamine 3- and 4-receptor, inhibited eosinophil infiltration to the esophagus in an allergen-inhalation model of EoE in guinea pigs. 89 In addition PGD2, a prostanoid largely produced by mast cells, is sufficient to drive eosinophils to the esophagus since injection of a PGD2 agonist into the esophagus led to rapid recruitment of eosinophils in guinea pigs, and pretreatment with a selective antagonist limited this experimental EoE-like disease. 90 Also, in adults with corticosteroid-resistant EoE, treatment for 8 weeks with OC000459, a selective antagonist of CRTH2, the receptor for PGD2, led to reduced tissue eosinophilia and clinical symptoms.…”

Section: Bodymentioning

confidence: 99%

Allergic Mechanisms in Eosinophilic Esophagitis

Wechsler

Bryce

2014

Gastroenterology Clinics of North America

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Paralleling the overall trend in allergic diseases, Eosinophilic Esophagitis is rapidly increasing in incidence. It is associated with food antigen-triggered, eosinophil-predominant inflammation and the pathogenic mechanisms have many similarities to other chronic atopic diseases, such as eczema and allergic asthma. Studies in animal models and from patients over the last 15 years have suggested that allergic sensitization leads to food-specific IgE and T-helper lymphocyte type 2 cells, both of which appear to contribute to the pathogenesis along with basophils, mast cells, and antigen-presenting cells. This review will outline our current understandings of the allergic mechanisms that drive eosinophilic esophagitis, drawing from clinical and translational studies in humans as well as experimental animal models.

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Section: Bodymentioning

confidence: 99%

Allergic Mechanisms in Eosinophilic Esophagitis

Wechsler

Bryce

2014

Gastroenterology Clinics of North America

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“…Yu et al showed that mast cell migration into the esophageal tissue precedes eosinophil migration in a guinea pig model of EoE. A histamine receptor antagonist, attenuated both mast cell and eosinophil migration in this model 60 , suggesting that granulocyte recruitment is in part due to a histamine mediated pathway. This, however, is in contrast to Niranjan et al, who showed in an aspergillus model of EoE that mice deficient in mast cells continue to have the same degree of eosinophilic infiltration as wild type mice 61 .…”

Section: Microenvironment Alterations In Eoementioning

confidence: 91%

Recent advances in the pathological understanding of eosinophilic esophagitis

Cianferoni

Spergel

Muir

2015

Expert Review of Gastroenterology & Hepatology

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Eosinophilic esophagitis (EoE) is a chronic allergen-mediated inflammatory disease of the esophagus. This inflammation leads to feeding difficulties, failure to thrive and vomiting in young children, and causes food impaction and esophageal stricture in adolescents and adults. In the twenty years since EoE was first described, we have gained a great deal of knowledge regarding the genetic predisposition of disease, the inflammatory mileu associated with EoE and the long term complications of chronic inflammation. Herein, we summarize the important breakthroughs in the field including both in vitro and in vivo analysis. We discuss insights that we have gained from large scale unbiased genetic analysis, a multitude of genetically and chemically altered mouse models of EoE and most importantly, the results of clinical trials of various pharmacologic agents. Understanding these successes and failures may be the key to developing more effective therapeutic strategies.

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“…49 Intraepithelial mast cell numbers are increased in EoE. 28,37,50,51 When aerosolized ovalbumin was used to induce esophageal eosinophilia in guinea pigs, mast cells preceded eosinophils into the epithelium, 52 as they do in other tissues. 53 Additionally, in this model, histamine release peaked 2 min after ovalbumin exposure and was followed by sustained C-fiber hyperexcitability.…”

Section: The Mast Cellmentioning

confidence: 99%

Understanding eosinophilic esophagitis: the cellular and molecular mechanisms of an emerging disease

Mulder

Justinich

2011

Mucosal Immunology

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Eosinophilic esophagitis (EoE) has been increasingly recognized as a unique clinicopathological entity over the past two decades. In this short time, the mechanisms of a complex disease have begun to emerge. Patient studies suggest that EoE is an immunologic disease related to atopy. At the cellular level, eosinophils, mast cells, and B and T lymphocytes are increased in the esophageal mucosa in a patchy distribution throughout the length of the esophagus. Laboratory investigations have implicated aeroallergens, food allergens, and a unique T helper type 2 cytokine profile. EoE appears to be an antigen-driven hypersensitivity reaction characterized by a mixed IgE-dependent/delayed-type reaction and a distinct cascade of cytokines and growth factors. The causative events that lead to EoE in humans remain unknown.

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Antigen inhalation induces mast cells and eosinophils infiltration in the guinea pig esophageal epithelium involving histamine-mediated pathway

Cited by 34 publications

References 39 publications

Allergic Mechanisms in Eosinophilic Esophagitis

Allergic Mechanisms in Eosinophilic Esophagitis

Recent advances in the pathological understanding of eosinophilic esophagitis

Understanding eosinophilic esophagitis: the cellular and molecular mechanisms of an emerging disease

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