Interplay of Adaptive Th2 Immunity with Eotaxin‐3/C‐C Chemokine Receptor 3 in Eosinophilic Esophagitis

Bullock, Jennifer Z.; Villanueva, Joyce; Blanchard, Carine; Filipovich, Alexandra H.; Putnam, Philip E.; Collins, Margaret H.; Risma, Kimberly A.; Akers, Rachel; Kirby, Cassie L.; Buckmeier, Bridget K.; Assa’ad, Amal; Hogan, Simon P.; Rothenberg, Marc E.

doi:10.1097/mpg.0b013e318043c097

Cited by 113 publications

(81 citation statements)

References 50 publications

(74 reference statements)

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“…IL-5 mRNA is increased in the biopsies of EE patients compared to NL patients ( (28,29) and unpublished data). Peripheral CD4+T cells show an increase in intracellular IL-5 in the blood of EE patients compared to non-atopic non-EE patients (10). Determining the role of IL-5 in EE is of importance since two independent studies have shown an improvement in the clinical and/or pathological symptoms of EE after anti-IL-5 treatment (30-32).…”

Section: Molecular Pathogenesismentioning

confidence: 99%

“…Thus, the immune responses in EE are characterized by enhanced production of Th2-associated cytokines in response to both food and environmental allergens. Finally, in a recent study examining intracellular staining of PBMC cytokines and cytokine production after stimulation in EE patients, the systemic parameters of EE patients were highly similar to atopic non-EE patients (10).…”

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confidence: 99%

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Basic Pathogenesis of Eosinophilic Esophagitis

Blanchard

Rothenberg

2008

Gastrointestinal Endoscopy Clinics of North America

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Section: Molecular Pathogenesismentioning

confidence: 99%

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confidence: 99%

Basic Pathogenesis of Eosinophilic Esophagitis

Blanchard

Rothenberg

2008

Gastrointestinal Endoscopy Clinics of North America

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“…Moreover, it has also been demonstrated that the inflammatory response in EoE patients is restricted to the esophagus and does not involve the stomach and/or duodenum [10]. The Th2-type inflammatory profile of EoE was subsequently confirmed in pediatric and adult EoE [12], and relevant allergens were identified for both pediatric and adult EoE [11,13]. Moreover, a strong link between atopy and EoE was subsequently described in both pediatric and adult EoE patient groups [14,15].…”

Section: Cells and Cytokinesmentioning

confidence: 99%

Immunopathogenesis of Eosinophilic Esophagitis

Simon

Straumann

2014

Dig Dis

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Background: Eosinophilic esophagitis (EoE) is a chronic inflammatory disease of the esophagus associated with dysphagia in adults and refractory reflux syndromes in children. Methods: Immunological and genetic approaches have been used to better understand the pathophysiology of the underlying inflammation. Results and Conclusions: Evidence has accumulated that EoE represents a T-helper (Th) 2-type inflammatory disease, in which allergens play a role in triggering the disease. The majority of the patients suffer from concurrent allergic rhinitis, asthma, and eczema, and have a history of atopy. The chronic inflammatory response in EoE is associated with tissue damage and remodeling, both of which lead to esophageal dysfunction and bolus impaction. The new insights into the pathophysiology have resulted in the development of the first pharmacological therapies of EoE.

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“…Genome-wide microarray expression studies have shown that the gene-encoding eotaxin-3 is the most highly induced gene in EoE patients compared to healthy individuals [43] . Furthermore, a single-nucleotide polymorphism in the human eotaxin-3 gene seems to be associated with disease susceptibility and mice deficient in the eotaxin receptor were protected from experimental EoE [63,64] . Eosinophils are born from the bone marrow progenitor stem cells under the influence of interleukin-3 (IL-3), interleukin-5 (IL-5) and granulocyte-macrophage colony-stimulating factor (GM-CSF).…”

Section: Genetic Vs Environmental Etiological Factorsmentioning

confidence: 99%

“…Similarly to GERD patients with esophagitis [60,61] , EoE is associated with high levels of cytokines particularly IL-3, IL-5, IL-13, increase production of eotaxin chemokines CCL11, CCL24 and CCL26 (or eotaxins 1, 2 and 3 respectively) that attract inflammatory cells, predominantly eosinophils [62,63] . Studies performed in esophageal rings showed that stimulation of the rings with IL-13 for 48 h resulted in a significant attraction of eosinophils into the lower chamber containing TH-2 lymphocytes while chambers containing only IL-13 did not [64,65] . These data demonstrate that IL-13 supports eosinophil migration and that CCL11 and CCL24 also are both important in promoting eosinophil infiltration [66,67] .…”

Section: Genetic Vs Environmental Etiological Factorsmentioning

confidence: 99%

Eosinophilic esophagitis: New insights in pathogenesis and therapy

Guarino

Cicala

Behar

2016

WJGPT

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Eosinophilic esophagitis (EoE) is a clinico-pathological entity with esophageal symptoms and dense esophageal eosinophilic infiltration throughout the esophagus that may persist despite treatment with proton pump inhibitors. This eosinophilic infiltration is usually absent in the stomach, small intestine and colon, although there are a number of reports of patients with a multiorgan involvement. EoE is associated with abnormalities involving TH2-dependent immunity, with multiple environmental factors strongly contributing to disease expression. The layer of the esophagus affected by the eosinophilic infiltration causes the specific symptoms. Esophageal involvement results mostly in dysphagia for solids that can be severe enough to cause recurrent esophageal obstruction with typical endoscopic features suggesting esophageal remodeling and pathological changes of eosinophilic infiltration of the mucosa, sub-epithelial fibrosis and muscle hypertrophy. This disease is frequently associated with other allergic conditions such as allergic asthma, allergic dermatitis and eosinophilia. The treatment of patients with EoE depends on the severity of the symptoms and of the inflammatory process as well as to their response to a gradual step-up treatment. The first line of treatment consists of steroid containing local inhalers. If unresponsive they are then treated with oral steroids. Intravenous interleukin blockers seem to have a consistent positive therapeutic effect. Core tip: Eosinophilic esophagitis is a clinico-pathological entity characterized by esophageal symptoms and dense esophageal eosinophilic infiltration throughout the esophagus. Our manuscript provides a deep description of the disease showing that many efforts have been made in the last decades in understanding REVIEWSubmit a

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Interplay of Adaptive Th2 Immunity with Eotaxin‐3/C‐C Chemokine Receptor 3 in Eosinophilic Esophagitis

Abstract: Collectively, these studies demonstrate cooperation between systemic CD4+ Th2-cell-mediated immunity and an enhanced eosinophil-CCR3/eotaxin-3 pathway in EE pathogenesis. Furthermore, the imbalanced Th2 immunity and increased CCR3 expression are reversible with disease remission.

Cited by 113 publications

References 50 publications

Basic Pathogenesis of Eosinophilic Esophagitis

Basic Pathogenesis of Eosinophilic Esophagitis

Immunopathogenesis of Eosinophilic Esophagitis

Eosinophilic esophagitis: New insights in pathogenesis and therapy

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