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Eosinophils in Eosinophilic Esophagitis: The Road to Fibrostenosis is Paved With Good Intentions
Frontiers in Immunology ( IF 5.7 ) Pub Date : 2020-11-03 , DOI: 10.3389/fimmu.2020.603295
Alfred D Doyle 1 , Mia Y Masuda 1 , Hirohito Kita 1, 2 , Benjamin L Wright 1, 3
Affiliation  

Eosinophilic esophagitis (EoE) is an antigen-driven disease associated with epithelial barrier dysfunction and chronic type 2 inflammation. Eosinophils are the defining feature of EoE histopathology but relatively little is known about their role in disease onset and progression. Classically defined as destructive, end-stage effector cells, eosinophils (a resident leukocyte in most of the GI tract) are increasingly understood to play roles in local immunity, tissue homeostasis, remodeling, and repair. Indeed, asymptomatic esophageal eosinophilia is observed in IgE-mediated food allergy. Interestingly, EoE is a potential complication of oral immunotherapy (OIT) for food allergy. However, we recently found that patients with peanut allergy may have asymptomatic esophageal eosinophilia at baseline and that peanut OIT induces transient esophageal eosinophilia in most subjects. This is seemingly at odds with multiple studies which have shown that EoE disease severity correlates with tissue eosinophilia. Herein, we review the potential role of eosinophils in EoE at different stages of disease pathogenesis. Based on current literature we suggest the following: (1) eosinophils are recruited to the esophagus as a homeostatic response to epithelial barrier disruption; (2) eosinophils mediate barrier-protective activities including local antibody production, mucus production and epithelial turnover; and (3) when type 2 inflammation persists, eosinophils promote fibrosis.



中文翻译:

嗜酸性粒细胞性食管炎中的嗜酸性粒细胞:纤维化狭窄的道路铺就了良好的意图

嗜酸性食管炎(EoE)是一种抗原驱动的疾病,与上皮屏障功能障碍和慢性2型炎症相关。嗜酸性粒细胞是EoE组织病理学的主要特征,但对其在疾病发作和进展中的作用了解甚少。嗜酸性粒细胞(大多数胃肠道中的常驻白细胞)被经典地定义为破坏性的,终末期的效应细胞,人们日益了解其在局部免疫,组织稳态,重塑和修复中的作用。实际上,在IgE介导的食物过敏中观察到无症状的食管嗜酸性粒细胞增多。有趣的是,EoE是口服免疫疗法(OIT)对食物过敏的潜在并发症。然而,我们最近发现,患有花生过敏的患者在基线时可能无症状性食管嗜酸性粒细胞增多,而花生OIT在大多数受试者中会诱发短暂性食管嗜酸粒细胞增多。这似乎与多项研究不一致,多项研究表明EoE疾病的严重程度与组织嗜酸性粒细胞增多有关。本文中,我们综述了嗜酸性粒细胞在疾病发病机理不同阶段在EoE中的潜在作用。根据目前的文献,我们提出以下建议:(1)嗜酸性粒细胞被募集到食道,作为对上皮屏障破坏的稳态反应;(2)嗜酸性粒细胞介导屏障保护活性,包括局部抗体产生,粘液产生和上皮周转;(3)当2型炎症持续存在时,嗜酸性粒细胞会促进纤维化。这似乎与多项研究不一致,多项研究表明EoE疾病的严重程度与组织嗜酸性粒细胞增多有关。本文中,我们综述了嗜酸性粒细胞在疾病发病机理不同阶段在EoE中的潜在作用。根据目前的文献,我们提出以下建议:(1)嗜酸性粒细胞被募集到食道,作为对上皮屏障破坏的稳态反应;(2)嗜酸性粒细胞介导屏障保护活性,包括局部抗体产生,粘液产生和上皮周转;(3)当2型炎症持续存在时,嗜酸性粒细胞会促进纤维化。这似乎与多项研究不一致,多项研究表明EoE疾病的严重程度与组织嗜酸性粒细胞增多有关。本文中,我们综述了嗜酸性粒细胞在疾病发病机理不同阶段在EoE中的潜在作用。根据目前的文献,我们提出以下建议:(1)嗜酸性粒细胞被募集到食道,作为对上皮屏障破坏的稳态反应;(2)嗜酸性粒细胞介导屏障保护活性,包括局部抗体产生,粘液产生和上皮周转;(3)当2型炎症持续存在时,嗜酸性粒细胞会促进纤维化。(1)将嗜酸性粒细胞募集到食道,作为对上皮屏障破坏的稳态反应;(2)嗜酸性粒细胞介导屏障保护活性,包括局部抗体产生,粘液产生和上皮周转;(3)当2型炎症持续存在时,嗜酸性粒细胞会促进纤维化。(1)将嗜酸性粒细胞募集到食道,作为对上皮屏障破坏的稳态反应;(2)嗜酸性粒细胞介导屏障保护活性,包括局部抗体产生,粘液产生和上皮周转;(3)当2型炎症持续存在时,嗜酸性粒细胞会促进纤维化。

更新日期:2020-12-01
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