title: Cytokine expression in normal and inflamed esophageal mucosa: a study into the pathogenesis of allergic eosinophilic esophagitis.
abstract: OBJECTIVE
  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 (>or=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)-gamma, interleukin (IL)-4, IL-5, IL-13, eotaxin-1, eotaxin-2, eotaxin-3, and RANTES was studied. IFN-gamma 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.
authors.affiliation: Indiana University, Indianapolis, Indiana, USA. sgupta@iupui.edu
authors.forename: Sandeep K
authors.initials: SK
authors.lastname: Gupta
authors.forename: Joseph F
authors.initials: JF
authors.lastname: Fitzgerald
authors.forename: Tamara
authors.initials: T
authors.lastname: Kondratyuk
authors.forename: Harm
authors.initials: H
authors.lastname: HogenEsch
mesh_terms: D000293:Adolescent; D016022:Case-Control Studies; D054413:Chemokine CCL11; D054423:Chemokine CCL24; D000075906:Chemokine CCL26; D019742:Chemokines, CC / Q000378:metabolism; D002648:Child; D002675:Child, Preschool; D004802:Eosinophilia / Q000209:etiology / Q000276:immunology*; D004804:Eosinophils / Q000502:physiology; D004941:Esophagitis / Q000209:etiology / Q000276:immunology*; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D007223:Infant; D007371:Interferon-gamma / Q000378:metabolism; D018793:Interleukin-13 / Q000096:biosynthesis; D015847:Interleukin-4 / Q000096:biosynthesis; D015848:Interleukin-5 / Q000096:biosynthesis*; D008297:Male; D008407:Mast Cells / Q000502:physiology; D016133:Polymerase Chain Reaction; D012333:RNA, Messenger / Q000378:metabolism*; D018417:Th1 Cells / Q000378:metabolism; D018418:Th2 Cells / Q000276:immunology*; D015854:Up-Regulation
chemical_list: C515456:CCL11 protein, human; C515484:CCL24 protein, human; C120429:CCL26 protein, human; D054413:Chemokine CCL11; D054423:Chemokine CCL24; D000075906:Chemokine CCL26; D019742:Chemokines, CC; D018793:Interleukin-13; D015848:Interleukin-5; D012333:RNA, Messenger; D015847:Interleukin-4; D007371:Interferon-gamma