{"title":"Esophageal remodeling in eosinophilic esophagitis.","authors":"Anisa Shaker","doi":"10.1097/MOG.0000000000001031","DOIUrl":null,"url":null,"abstract":"PURPOSE OF REVIEW\nEosinophilic esophagitis (EoE) is a Th2 immune/antigen-mediated disorder characterized by esophageal dysfunction and eosinophilic inflammation. Worsening dysphagia and food impactions are significant complications associated with esophageal remodeling and fibrostenotic disease. This review highlights the most recent research findings pertaining to mechanisms of sub-epithelial fibrosis in EoE, current diagnostic tools, and therapeutic approaches.\n\n\nRECENT FINDINGS\nRecent studies leveraging publicly available single cell sequencing databases and comparative proteomics have furthered our understanding of the mechanisms mediating fibrosis. Fibroblast crosstalk with the extracellular matrix and with epithelial, endothelial, and T cells have been implicated, with the likely existence of multiple fibroblast sub-types. Accurate diagnosis of remodeling with biopsies remains a challenge due to inadequate depth of sampling. Web-based tools incorporating epithelial findings show promise in predicting subepithelial fibrosis. Impedance planimetry with esophageal distensibility measurements are increasingly utilized tools to assess fibrostenotic severity. Immunostaining and luminal captured proteins associated with remodeling show promise as potential molecular markers of fibrosis. Anti-inflammatory therapy may improve esophageal fibrosis and distensibility, although specific fibrosis-targeted therapy is lacking.\n\n\nSUMMARY\nRecent studies highlight novel mechanisms of fibrosis in EoE. Improved understanding of these mechanisms may lead to novel diagnostic strategies and therapies, and thereby inform treatment decisions.","PeriodicalId":50607,"journal":{"name":"Current Opinion in Gastroenterology","volume":null,"pages":null},"PeriodicalIF":2.6000,"publicationDate":"2024-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Current Opinion in Gastroenterology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1097/MOG.0000000000001031","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"GASTROENTEROLOGY & HEPATOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
PURPOSE OF REVIEW
Eosinophilic esophagitis (EoE) is a Th2 immune/antigen-mediated disorder characterized by esophageal dysfunction and eosinophilic inflammation. Worsening dysphagia and food impactions are significant complications associated with esophageal remodeling and fibrostenotic disease. This review highlights the most recent research findings pertaining to mechanisms of sub-epithelial fibrosis in EoE, current diagnostic tools, and therapeutic approaches.
RECENT FINDINGS
Recent studies leveraging publicly available single cell sequencing databases and comparative proteomics have furthered our understanding of the mechanisms mediating fibrosis. Fibroblast crosstalk with the extracellular matrix and with epithelial, endothelial, and T cells have been implicated, with the likely existence of multiple fibroblast sub-types. Accurate diagnosis of remodeling with biopsies remains a challenge due to inadequate depth of sampling. Web-based tools incorporating epithelial findings show promise in predicting subepithelial fibrosis. Impedance planimetry with esophageal distensibility measurements are increasingly utilized tools to assess fibrostenotic severity. Immunostaining and luminal captured proteins associated with remodeling show promise as potential molecular markers of fibrosis. Anti-inflammatory therapy may improve esophageal fibrosis and distensibility, although specific fibrosis-targeted therapy is lacking.
SUMMARY
Recent studies highlight novel mechanisms of fibrosis in EoE. Improved understanding of these mechanisms may lead to novel diagnostic strategies and therapies, and thereby inform treatment decisions.
综述目的嗜酸性粒细胞食管炎(EoE)是一种 Th2 免疫/抗原介导的疾病,其特征是食管功能障碍和嗜酸性粒细胞炎症。吞咽困难和食物嵌塞是与食管重塑和纤维增生性疾病相关的重要并发症。本综述重点介绍了有关食管上皮下纤维化机制、当前诊断工具和治疗方法的最新研究成果。最近的发现最近的研究利用公开的单细胞测序数据库和比较蛋白质组学进一步加深了我们对纤维化介导机制的了解。成纤维细胞与细胞外基质以及上皮细胞、内皮细胞和 T 细胞之间的串扰已被证实,并可能存在多种成纤维细胞亚型。由于取样深度不够,利用活检对重塑进行准确诊断仍是一项挑战。结合上皮发现的网络工具在预测上皮下纤维化方面大有可为。阻抗平面测量法和食管扩张性测量法越来越多地被用来评估纤维化的严重程度。与重塑相关的免疫染色和管腔捕获蛋白有望成为潜在的纤维化分子标记物。抗炎治疗可改善食管纤维化和扩张性,但目前还缺乏针对纤维化的特异性疗法。对这些机制的进一步了解可能会带来新的诊断策略和疗法,从而为治疗决策提供依据。
期刊介绍:
Published bimonthly and offering a unique and wide ranging perspective on the key developments in the field, each issue of Current Opinion in Gastroenterology features hand-picked review articles from our team of expert editors. With twelve disciplines published across the year – including gastrointestinal infections, nutrition and inflammatory bowel disease – every issue also contains annotated references detailing the merits of the most important papers.