Eosinophilic esophagitis: Immune mechanisms and therapeutic targets
Eosinophilic esophagitis (EoE) is an emerging chronic inflammatory disease of the oesophagus and is clinically characterized by upper gastrointestinal (GI) symptoms including dysphagia and esophageal food impaction. Histopathologic manifestations, which include intraepithelial eosinophilic inflammat...
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| Veröffentlicht in: | Clinical and experimental allergy 2022-10, Vol.52 (10), p.1142-1156 |
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| creator | Khokhar, Dilawar Marella, Sahiti Idelman, Gila Chang, Joy W. Chehade, Mirna Hogan, Simon P. |
| description | Eosinophilic esophagitis (EoE) is an emerging chronic inflammatory disease of the oesophagus and is clinically characterized by upper gastrointestinal (GI) symptoms including dysphagia and esophageal food impaction. Histopathologic manifestations, which include intraepithelial eosinophilic inflammation and alterations of the esophageal squamous epithelium, such as basal zone hyperplasia (BZH) and dilated intercellular spaces (DIS), are thought to contribute to esophageal dysfunction and disease symptoms. Corroborative clinical and discovery science‐based studies have established that EoE is characterized by an underlying allergic inflammatory response, in part, related to the IL‐13/CCL26/eosinophil axis driving dysregulation of several key epithelial barrier and proliferative regulatory genes including kallikrein (KLK) serine proteases, calpain 14 (CAPN14) and anoctamin 1 (ANO1). The contribution of these inflammatory and proliferative processes to the clinical and histological manifestations of disease are not fully elucidated. Herein, we discuss the immune molecules and cells that are thought to underlie the clinical and pathologic manifestations of EoE and the emerging therapeutics targeting these processes for the treatment of EoE. |
| doi_str_mv | 10.1111/cea.14196 |
| format | Article |
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Histopathologic manifestations, which include intraepithelial eosinophilic inflammation and alterations of the esophageal squamous epithelium, such as basal zone hyperplasia (BZH) and dilated intercellular spaces (DIS), are thought to contribute to esophageal dysfunction and disease symptoms. Corroborative clinical and discovery science‐based studies have established that EoE is characterized by an underlying allergic inflammatory response, in part, related to the IL‐13/CCL26/eosinophil axis driving dysregulation of several key epithelial barrier and proliferative regulatory genes including kallikrein (KLK) serine proteases, calpain 14 (CAPN14) and anoctamin 1 (ANO1). The contribution of these inflammatory and proliferative processes to the clinical and histological manifestations of disease are not fully elucidated. Herein, we discuss the immune molecules and cells that are thought to underlie the clinical and pathologic manifestations of EoE and the emerging therapeutics targeting these processes for the treatment of EoE.</description><identifier>ISSN: 0954-7894</identifier><identifier>EISSN: 1365-2222</identifier><identifier>DOI: 10.1111/cea.14196</identifier><identifier>PMID: 35778876</identifier><language>eng</language><publisher>England: Wiley Subscription Services, Inc</publisher><subject>Anoctamin-1 ; Autoimmune diseases ; biologics ; Calpain ; cytokines ; Dysphagia ; eosinophilic esophagitis ; Eosinophilic Esophagitis - drug therapy ; Eosinophilic Esophagitis - therapy ; Eosinophils ; Epithelium ; Esophageal diseases ; Esophagitis ; Esophagus ; Gastrointestinal diseases ; Humans ; Hyperplasia ; Hypersensitivity ; Inflammatory diseases ; Interleukin-13 - metabolism ; Kallikrein ; Kallikreins ; Leukocytes (eosinophilic) ; mast cell ; Review ; Serine Proteases ; Serine proteinase ; Therapeutic targets</subject><ispartof>Clinical and experimental allergy, 2022-10, Vol.52 (10), p.1142-1156</ispartof><rights>2022 The Authors. published by John Wiley & Sons Ltd.</rights><rights>2022 The Authors. 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Histopathologic manifestations, which include intraepithelial eosinophilic inflammation and alterations of the esophageal squamous epithelium, such as basal zone hyperplasia (BZH) and dilated intercellular spaces (DIS), are thought to contribute to esophageal dysfunction and disease symptoms. Corroborative clinical and discovery science‐based studies have established that EoE is characterized by an underlying allergic inflammatory response, in part, related to the IL‐13/CCL26/eosinophil axis driving dysregulation of several key epithelial barrier and proliferative regulatory genes including kallikrein (KLK) serine proteases, calpain 14 (CAPN14) and anoctamin 1 (ANO1). The contribution of these inflammatory and proliferative processes to the clinical and histological manifestations of disease are not fully elucidated. Herein, we discuss the immune molecules and cells that are thought to underlie the clinical and pathologic manifestations of EoE and the emerging therapeutics targeting these processes for the treatment of EoE.</description><subject>Anoctamin-1</subject><subject>Autoimmune diseases</subject><subject>biologics</subject><subject>Calpain</subject><subject>cytokines</subject><subject>Dysphagia</subject><subject>eosinophilic esophagitis</subject><subject>Eosinophilic Esophagitis - drug therapy</subject><subject>Eosinophilic Esophagitis - therapy</subject><subject>Eosinophils</subject><subject>Epithelium</subject><subject>Esophageal diseases</subject><subject>Esophagitis</subject><subject>Esophagus</subject><subject>Gastrointestinal diseases</subject><subject>Humans</subject><subject>Hyperplasia</subject><subject>Hypersensitivity</subject><subject>Inflammatory diseases</subject><subject>Interleukin-13 - metabolism</subject><subject>Kallikrein</subject><subject>Kallikreins</subject><subject>Leukocytes (eosinophilic)</subject><subject>mast cell</subject><subject>Review</subject><subject>Serine Proteases</subject><subject>Serine proteinase</subject><subject>Therapeutic targets</subject><issn>0954-7894</issn><issn>1365-2222</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>EIF</sourceid><recordid>eNp1kctKLDEURYMo2j4G_oAUOLl3UJpXJSkHgjTtAwQnOg6nKsfuSD3apErpv7_xtooKnkkCWSx2zibkkNETlua0RjhhkpVqg0yYUEXO02ySCS0LmWtTyh2yG-MTpVQUpdkmO6LQ2hitJmQ666Pv-uXCN77OMKYbzP3g41l207Zjh1mL9QI6H9uYQeeyYYEBljgOCR8gzHGI-2TrEZqIB-_nHnm4nN1Pr_Pbu6ub6cVtXkspVM5RFxVIZUpBK4AUBTVzlGp0jjNwRsqKSwpK1QI4r5h2WGgnBTNAlQOxR87X3uVYtehq7IYAjV0G30JY2R68_f7S-YWd9y82rUEbwZPgz7sg9M8jxsG2PtbYNNBhP0bLlZG0VEyrhB7_QJ_6MXTpe5ZrztKWGS8S9XdN1aGPMeDjZxhG7Vs1NlVj_1eT2KOv6T_Jjy4ScLoGXn2Dq99Ndjq7WCv_AfyvmHc</recordid><startdate>202210</startdate><enddate>202210</enddate><creator>Khokhar, Dilawar</creator><creator>Marella, Sahiti</creator><creator>Idelman, Gila</creator><creator>Chang, Joy W.</creator><creator>Chehade, Mirna</creator><creator>Hogan, Simon P.</creator><general>Wiley Subscription Services, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>202210</creationdate><title>Eosinophilic esophagitis: Immune mechanisms and therapeutic targets</title><author>Khokhar, Dilawar ; Marella, Sahiti ; Idelman, Gila ; Chang, Joy W. ; Chehade, Mirna ; Hogan, Simon P.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4436-2e75ba468930baa359e71d007edd21ad844b240a66c3a22b17de57d4318a06da3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Anoctamin-1</topic><topic>Autoimmune diseases</topic><topic>biologics</topic><topic>Calpain</topic><topic>cytokines</topic><topic>Dysphagia</topic><topic>eosinophilic esophagitis</topic><topic>Eosinophilic Esophagitis - drug therapy</topic><topic>Eosinophilic Esophagitis - therapy</topic><topic>Eosinophils</topic><topic>Epithelium</topic><topic>Esophageal diseases</topic><topic>Esophagitis</topic><topic>Esophagus</topic><topic>Gastrointestinal diseases</topic><topic>Humans</topic><topic>Hyperplasia</topic><topic>Hypersensitivity</topic><topic>Inflammatory diseases</topic><topic>Interleukin-13 - metabolism</topic><topic>Kallikrein</topic><topic>Kallikreins</topic><topic>Leukocytes (eosinophilic)</topic><topic>mast cell</topic><topic>Review</topic><topic>Serine Proteases</topic><topic>Serine proteinase</topic><topic>Therapeutic targets</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Khokhar, Dilawar</creatorcontrib><creatorcontrib>Marella, Sahiti</creatorcontrib><creatorcontrib>Idelman, Gila</creatorcontrib><creatorcontrib>Chang, Joy W.</creatorcontrib><creatorcontrib>Chehade, Mirna</creatorcontrib><creatorcontrib>Hogan, Simon P.</creatorcontrib><collection>Wiley Online Library Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Clinical and experimental allergy</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Khokhar, Dilawar</au><au>Marella, Sahiti</au><au>Idelman, Gila</au><au>Chang, Joy W.</au><au>Chehade, Mirna</au><au>Hogan, Simon P.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Eosinophilic esophagitis: Immune mechanisms and therapeutic targets</atitle><jtitle>Clinical and experimental allergy</jtitle><addtitle>Clin Exp Allergy</addtitle><date>2022-10</date><risdate>2022</risdate><volume>52</volume><issue>10</issue><spage>1142</spage><epage>1156</epage><pages>1142-1156</pages><issn>0954-7894</issn><eissn>1365-2222</eissn><abstract>Eosinophilic esophagitis (EoE) is an emerging chronic inflammatory disease of the oesophagus and is clinically characterized by upper gastrointestinal (GI) symptoms including dysphagia and esophageal food impaction. Histopathologic manifestations, which include intraepithelial eosinophilic inflammation and alterations of the esophageal squamous epithelium, such as basal zone hyperplasia (BZH) and dilated intercellular spaces (DIS), are thought to contribute to esophageal dysfunction and disease symptoms. Corroborative clinical and discovery science‐based studies have established that EoE is characterized by an underlying allergic inflammatory response, in part, related to the IL‐13/CCL26/eosinophil axis driving dysregulation of several key epithelial barrier and proliferative regulatory genes including kallikrein (KLK) serine proteases, calpain 14 (CAPN14) and anoctamin 1 (ANO1). The contribution of these inflammatory and proliferative processes to the clinical and histological manifestations of disease are not fully elucidated. 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| subjects | Anoctamin-1 Autoimmune diseases biologics Calpain cytokines Dysphagia eosinophilic esophagitis Eosinophilic Esophagitis - drug therapy Eosinophilic Esophagitis - therapy Eosinophils Epithelium Esophageal diseases Esophagitis Esophagus Gastrointestinal diseases Humans Hyperplasia Hypersensitivity Inflammatory diseases Interleukin-13 - metabolism Kallikrein Kallikreins Leukocytes (eosinophilic) mast cell Review Serine Proteases Serine proteinase Therapeutic targets |
| title | Eosinophilic esophagitis: Immune mechanisms and therapeutic targets |
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