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 |
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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. |
doi_str_mv | 10.1097/01.mpg.0000188740.38757.d2 |
format | Article |
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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.</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 & 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. 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</subject><ispartof>Journal of pediatric gastroenterology and nutrition, 2006-01, Vol.42 (1), p.22-26</ispartof><rights>2006 by European Society for European Society for Pediatric Gastroenterology, Hepatology, and Nutrition and North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition</rights><rights>2006 Lippincott Williams & Wilkins, Inc.</rights><rights>2006 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5339-9d8e1a485af65fda2f99c8570b5fc99cf6e75bcf1d85590c1eec2752ca9aa0a53</citedby><cites>FETCH-LOGICAL-c5339-9d8e1a485af65fda2f99c8570b5fc99cf6e75bcf1d85590c1eec2752ca9aa0a53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1097%2F01.mpg.0000188740.38757.d2$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1097%2F01.mpg.0000188740.38757.d2$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>309,310,314,780,784,789,790,1417,4050,4051,23930,23931,25140,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17439453$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16385249$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gupta, Sandeep K</creatorcontrib><creatorcontrib>Fitzgerald, Joseph F</creatorcontrib><creatorcontrib>Kondratyuk, Tamara</creatorcontrib><creatorcontrib>HogenEsch, Harm</creatorcontrib><title>Cytokine Expression in Normal and Inflamed Esophageal Mucosa: A Study into the Pathogenesis of Allergic Eosinophilic Esophagitis</title><title>Journal of pediatric gastroenterology and nutrition</title><addtitle>J Pediatr Gastroenterol Nutr</addtitle><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.</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 & 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. Feeding behavior</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Infant</topic><topic>Interferon-gamma - metabolism</topic><topic>Interleukin-13 - biosynthesis</topic><topic>Interleukin-4 - biosynthesis</topic><topic>Interleukin-5 - biosynthesis</topic><topic>Male</topic><topic>Mast Cells - physiology</topic><topic>Medical sciences</topic><topic>Other diseases. 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 & 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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