Cytokine Expression in Normal and Inflamed Esophageal Mucosa: A Study into the Pathogenesis of Allergic Eosinophilic Esophagitis

ABSTRACT Objectives: We studied the expression of cytokines and inflammatory cells in normal and inflamed esophageal mucosa of children with the aim of furthering our understanding of the pathophysiology of allergic eosinophilic esophagitis (AEE). Methods: Controls and AEE patients (≥15 eosinophils/...

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Veröffentlicht in:Journal of pediatric gastroenterology and nutrition 2006-01, Vol.42 (1), p.22-26
Hauptverfasser: Gupta, Sandeep K, Fitzgerald, Joseph F, Kondratyuk, Tamara, HogenEsch, Harm
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creator Gupta, Sandeep K
Fitzgerald, Joseph F
Kondratyuk, Tamara
HogenEsch, Harm
description ABSTRACT Objectives: We studied the expression of cytokines and inflammatory cells in normal and inflamed esophageal mucosa of children with the aim of furthering our understanding of the pathophysiology of allergic eosinophilic esophagitis (AEE). Methods: Controls and AEE patients (≥15 eosinophils/high‐power field on esophageal mucosal biopsies) between the ages of 1 and 18 years were recruited. Esophageal biopsies were obtained for histologic examination, immunohistochemical studies, and cytokine analysis. Results: Eight controls (4 males; mean age 9.99 years) and 11 AEE patients (8 males; mean age 7.15 years) were studied. mRNA expression of interferon (IFN)‐γ, interleukin (IL)‐4, IL‐5, IL‐13, eotaxin‐1, eotaxin‐2, eotaxin‐3, and RANTES was studied. IFN‐γ and IL‐5 expressions were significantly up‐regulated in AEE patients compared with controls. Expressions of IL‐4 and IL‐13 were similar between AEE patients and controls. Eotaxin‐1 expression was significantly up‐regulated in AEE patients, whereas eotaxin‐2 was up‐regulated in controls. Expression of RANTES and eotaxin‐3 was similar between the two groups. There was increased staining for mast cells in AEE patients compared with controls. Conclusions: Our data suggests that AEE is primarily an IL‐5 selective TH2 response, with a possible TH1 component, and a differential role of eosinophilic chemoattractants. The role of mast cells in the pathogenesis of AEE needs additional study.
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Methods: Controls and AEE patients (≥15 eosinophils/high‐power field on esophageal mucosal biopsies) between the ages of 1 and 18 years were recruited. Esophageal biopsies were obtained for histologic examination, immunohistochemical studies, and cytokine analysis. Results: Eight controls (4 males; mean age 9.99 years) and 11 AEE patients (8 males; mean age 7.15 years) were studied. mRNA expression of interferon (IFN)‐γ, interleukin (IL)‐4, IL‐5, IL‐13, eotaxin‐1, eotaxin‐2, eotaxin‐3, and RANTES was studied. IFN‐γ and IL‐5 expressions were significantly up‐regulated in AEE patients compared with controls. Expressions of IL‐4 and IL‐13 were similar between AEE patients and controls. Eotaxin‐1 expression was significantly up‐regulated in AEE patients, whereas eotaxin‐2 was up‐regulated in controls. Expression of RANTES and eotaxin‐3 was similar between the two groups. There was increased staining for mast cells in AEE patients compared with controls. Conclusions: Our data suggests that AEE is primarily an IL‐5 selective TH2 response, with a possible TH1 component, and a differential role of eosinophilic chemoattractants. The role of mast cells in the pathogenesis of AEE needs additional study.</description><identifier>ISSN: 0277-2116</identifier><identifier>EISSN: 1536-4801</identifier><identifier>DOI: 10.1097/01.mpg.0000188740.38757.d2</identifier><identifier>PMID: 16385249</identifier><identifier>CODEN: JPGND6</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams &amp; Wilkins, Inc</publisher><subject>Adolescent ; Allergic eosinophilic esophagitis ; Biological and medical sciences ; Case-Control Studies ; Chemokine CCL11 ; Chemokine CCL24 ; Chemokine CCL26 ; Chemokines, CC - metabolism ; Child ; Child, Preschool ; Cytokines ; Eosinophilia - etiology ; Eosinophilia - immunology ; Eosinophils - physiology ; Esophagitis - etiology ; Esophagitis - immunology ; Esophagus ; Feeding. Feeding behavior ; Female ; Fundamental and applied biological sciences. Psychology ; Gastroenterology. Liver. Pancreas. Abdomen ; Humans ; Immunohistochemistry ; Infant ; Interferon-gamma - metabolism ; Interleukin-13 - biosynthesis ; Interleukin-4 - biosynthesis ; Interleukin-5 - biosynthesis ; Male ; Mast Cells - physiology ; Medical sciences ; Other diseases. 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Methods: Controls and AEE patients (≥15 eosinophils/high‐power field on esophageal mucosal biopsies) between the ages of 1 and 18 years were recruited. Esophageal biopsies were obtained for histologic examination, immunohistochemical studies, and cytokine analysis. Results: Eight controls (4 males; mean age 9.99 years) and 11 AEE patients (8 males; mean age 7.15 years) were studied. mRNA expression of interferon (IFN)‐γ, interleukin (IL)‐4, IL‐5, IL‐13, eotaxin‐1, eotaxin‐2, eotaxin‐3, and RANTES was studied. IFN‐γ and IL‐5 expressions were significantly up‐regulated in AEE patients compared with controls. Expressions of IL‐4 and IL‐13 were similar between AEE patients and controls. Eotaxin‐1 expression was significantly up‐regulated in AEE patients, whereas eotaxin‐2 was up‐regulated in controls. Expression of RANTES and eotaxin‐3 was similar between the two groups. There was increased staining for mast cells in AEE patients compared with controls. Conclusions: Our data suggests that AEE is primarily an IL‐5 selective TH2 response, with a possible TH1 component, and a differential role of eosinophilic chemoattractants. The role of mast cells in the pathogenesis of AEE needs additional study.</description><subject>Adolescent</subject><subject>Allergic eosinophilic esophagitis</subject><subject>Biological and medical sciences</subject><subject>Case-Control Studies</subject><subject>Chemokine CCL11</subject><subject>Chemokine CCL24</subject><subject>Chemokine CCL26</subject><subject>Chemokines, CC - metabolism</subject><subject>Child</subject><subject>Child, Preschool</subject><subject>Cytokines</subject><subject>Eosinophilia - etiology</subject><subject>Eosinophilia - immunology</subject><subject>Eosinophils - physiology</subject><subject>Esophagitis - etiology</subject><subject>Esophagitis - immunology</subject><subject>Esophagus</subject><subject>Feeding. Feeding behavior</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Infant</subject><subject>Interferon-gamma - metabolism</subject><subject>Interleukin-13 - biosynthesis</subject><subject>Interleukin-4 - biosynthesis</subject><subject>Interleukin-5 - biosynthesis</subject><subject>Male</subject><subject>Mast Cells - physiology</subject><subject>Medical sciences</subject><subject>Other diseases. Semiology</subject><subject>Pediatrics</subject><subject>Polymerase Chain Reaction</subject><subject>RNA, Messenger - metabolism</subject><subject>Th1 Cells - metabolism</subject><subject>Th2 Cells - immunology</subject><subject>Up-Regulation</subject><subject>Vertebrates: anatomy and physiology, studies on body, several organs or systems</subject><issn>0277-2116</issn><issn>1536-4801</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqVkE9v0zAYhy0EYqXwFZCFBLcE_42T3UrVwdAYk4Cz5Tp2Y-bGmZ1o9MZHx10j9Ywv9ms9v_e1HwDeYVRi1IiPCJf7YVeivHBdC4ZKWgsuypY8AwvMaVWwGuHnYIGIEAXBuLoAr1L6nXnBOHoJLnBFa05YswB_14cx3LvewM2fIZqUXOih6-FtiHvloepbeN1br_amhZsUhk7tTL7_NumQ1CVcwR_j1B5yYgxw7Ay8U2MXdqY3ySUYLFx5b-LOabgJyfU57_yxOHVyo0uvwQurfDJv5n0Jfl1tfq6_FDffP1-vVzeF5pQ2RdPWBitWc2UrbltFbNPomgu05Vbno62M4FttcVtz3iCNjdFEcKJVoxRSnC7Bh1PfIYaHyaRR7l3SxnvVmzAlWYkKIYJYBi9PoI4hpWisHKLbq3iQGMmjf4mwzP7l2b988i9bksNv5ynTNis7R2fhGXg_Aypp5W1UvXbpzAlGG5Z_vATsxD0GP5qY7v30aKLssvyxexrNsagKglCFcK6K49Wx_XqOOW8O__Fy-fXuln66QlRUjP4DJ6e1Gg</recordid><startdate>200601</startdate><enddate>200601</enddate><creator>Gupta, Sandeep K</creator><creator>Fitzgerald, Joseph F</creator><creator>Kondratyuk, Tamara</creator><creator>HogenEsch, Harm</creator><general>Lippincott Williams &amp; Wilkins, Inc</general><general>Lippincott</general><scope>IQODW</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>7X8</scope></search><sort><creationdate>200601</creationdate><title>Cytokine Expression in Normal and Inflamed Esophageal Mucosa: A Study into the Pathogenesis of Allergic Eosinophilic Esophagitis</title><author>Gupta, Sandeep K ; Fitzgerald, Joseph F ; Kondratyuk, Tamara ; HogenEsch, Harm</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5339-9d8e1a485af65fda2f99c8570b5fc99cf6e75bcf1d85590c1eec2752ca9aa0a53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Adolescent</topic><topic>Allergic eosinophilic esophagitis</topic><topic>Biological and medical sciences</topic><topic>Case-Control Studies</topic><topic>Chemokine CCL11</topic><topic>Chemokine CCL24</topic><topic>Chemokine CCL26</topic><topic>Chemokines, CC - metabolism</topic><topic>Child</topic><topic>Child, Preschool</topic><topic>Cytokines</topic><topic>Eosinophilia - etiology</topic><topic>Eosinophilia - immunology</topic><topic>Eosinophils - physiology</topic><topic>Esophagitis - etiology</topic><topic>Esophagitis - immunology</topic><topic>Esophagus</topic><topic>Feeding. 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Semiology</topic><topic>Pediatrics</topic><topic>Polymerase Chain Reaction</topic><topic>RNA, Messenger - metabolism</topic><topic>Th1 Cells - metabolism</topic><topic>Th2 Cells - immunology</topic><topic>Up-Regulation</topic><topic>Vertebrates: anatomy and physiology, studies on body, several organs or systems</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gupta, Sandeep K</creatorcontrib><creatorcontrib>Fitzgerald, Joseph F</creatorcontrib><creatorcontrib>Kondratyuk, Tamara</creatorcontrib><creatorcontrib>HogenEsch, Harm</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of pediatric gastroenterology and nutrition</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gupta, Sandeep K</au><au>Fitzgerald, Joseph F</au><au>Kondratyuk, Tamara</au><au>HogenEsch, Harm</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cytokine Expression in Normal and Inflamed Esophageal Mucosa: A Study into the Pathogenesis of Allergic Eosinophilic Esophagitis</atitle><jtitle>Journal of pediatric gastroenterology and nutrition</jtitle><addtitle>J Pediatr Gastroenterol Nutr</addtitle><date>2006-01</date><risdate>2006</risdate><volume>42</volume><issue>1</issue><spage>22</spage><epage>26</epage><pages>22-26</pages><issn>0277-2116</issn><eissn>1536-4801</eissn><coden>JPGND6</coden><abstract>ABSTRACT Objectives: We studied the expression of cytokines and inflammatory cells in normal and inflamed esophageal mucosa of children with the aim of furthering our understanding of the pathophysiology of allergic eosinophilic esophagitis (AEE). Methods: Controls and AEE patients (≥15 eosinophils/high‐power field on esophageal mucosal biopsies) between the ages of 1 and 18 years were recruited. Esophageal biopsies were obtained for histologic examination, immunohistochemical studies, and cytokine analysis. Results: Eight controls (4 males; mean age 9.99 years) and 11 AEE patients (8 males; mean age 7.15 years) were studied. mRNA expression of interferon (IFN)‐γ, interleukin (IL)‐4, IL‐5, IL‐13, eotaxin‐1, eotaxin‐2, eotaxin‐3, and RANTES was studied. IFN‐γ and IL‐5 expressions were significantly up‐regulated in AEE patients compared with controls. Expressions of IL‐4 and IL‐13 were similar between AEE patients and controls. Eotaxin‐1 expression was significantly up‐regulated in AEE patients, whereas eotaxin‐2 was up‐regulated in controls. Expression of RANTES and eotaxin‐3 was similar between the two groups. There was increased staining for mast cells in AEE patients compared with controls. Conclusions: Our data suggests that AEE is primarily an IL‐5 selective TH2 response, with a possible TH1 component, and a differential role of eosinophilic chemoattractants. The role of mast cells in the pathogenesis of AEE needs additional study.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams &amp; Wilkins, Inc</pub><pmid>16385249</pmid><doi>10.1097/01.mpg.0000188740.38757.d2</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record>
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subjects Adolescent
Allergic eosinophilic esophagitis
Biological and medical sciences
Case-Control Studies
Chemokine CCL11
Chemokine CCL24
Chemokine CCL26
Chemokines, CC - metabolism
Child
Child, Preschool
Cytokines
Eosinophilia - etiology
Eosinophilia - immunology
Eosinophils - physiology
Esophagitis - etiology
Esophagitis - immunology
Esophagus
Feeding. Feeding behavior
Female
Fundamental and applied biological sciences. Psychology
Gastroenterology. Liver. Pancreas. Abdomen
Humans
Immunohistochemistry
Infant
Interferon-gamma - metabolism
Interleukin-13 - biosynthesis
Interleukin-4 - biosynthesis
Interleukin-5 - biosynthesis
Male
Mast Cells - physiology
Medical sciences
Other diseases. Semiology
Pediatrics
Polymerase Chain Reaction
RNA, Messenger - metabolism
Th1 Cells - metabolism
Th2 Cells - immunology
Up-Regulation
Vertebrates: anatomy and physiology, studies on body, several organs or systems
title Cytokine Expression in Normal and Inflamed Esophageal Mucosa: A Study into the Pathogenesis of Allergic Eosinophilic Esophagitis
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