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Review
. 2014 May;112(5):397-403.
doi: 10.1016/j.anai.2014.01.023. Epub 2014 Feb 22.

Eosinophilic esophagitis

Jamie Merves  1 , Amanda Muir  1 , Prasanna Modayur Chandramouleeswaran  1 , Antonella Cianferoni  2 , Mei-Lun Wang  1 , Jonathan M Spergel  3
Affiliations
Review

Eosinophilic esophagitis

Jamie Merves et al. Ann Allergy Asthma Immunol. 2014 May.

Abstract

Objective: To review the understanding of the pathogenesis of eosinophilic esophagitis (EoE) and the role of the immune system in the disease process.

Data sources: Peer-reviewed articles on EoE from PubMed searching for "Eosinophilic Esophagitis and fibrosis" in the period of 1995 to 2013.

Study selections: Studies on the clinical and immunologic features, pathogenesis, and management of EoE.

Results: Recent work has revealed that thymic stromal lymphopoietin and basophil have an increased role in the pathogenesis of disease. Additional understanding on the role of fibrosis in EoE is emerging.

Conclusion: The incidence of EoE is increasing like most atopic disease. Similar to other allergic diseases, EoE is treated with topical steroids and/or allergen avoidance.

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Figures

Figure 1
Figure 1
Mechanism of eosinophilic esophagitis pathogenesis. In genetically susceptible individuals, antigens (eg, allergen and infectious agents) and irritants (eg, acid reflux) induce esophageal epithelium to produce thymic stromal lymphopoietin (TSLP), interleukin (IL) 33, and eotaxin-3 (CCL-26). Eotaxin 3 (CCL-26) recruits eosinophils to the esophageal epithelium, whereas TSLP and IL-33 lead to dendritic cell and basophil activation and TH2 polarization. This results in TH2 cytokine (eg, IL-4, IL-5, and IL-13) secretion and the development of typical TH2 inflammation characterized by eosinophils, mast cells, and T cells. IL-5 further promotes expansion and survival of the recruited eosinophils, which in turn secrete IL-9 and IL-1β. Finally, IL-9 enhances mast cell activation, transforming growth factor β, and tumor necrosis factor α secretion and together with IL-1β induces myofibroblast differentiation and ultimately fibrosis.
Figure 2
Figure 2
Origin and function of the activated myofibroblast. Profibrotic cytokines, such as transforming growth factor β, tumor necrosis factor α, and interleukin 1, secreted in the setting of chronic inflammation activate epithelial cells, fibroblasts, and circulating fibrocytes and induce their transdifferentiation to a myofibroblast phenotype. These activated myofibroblasts contribute to the development of esophageal fibrosis because they produce α-smooth muscle actin, secrete collagen, and contract.
See this image and copyright information in PMC

References

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