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The Journal of Allergy and Clinical Immunology
Volume 119, Issue 1
, Pages
206-212
, January 2007
Esophageal remodeling in pediatric eosinophilic esophagitis
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Pediatric patients with EE have increased subepithelial fibrosis and TGF-β1. A-D, Trichrome stain of normal, GERD, EE esophageal biopsies and fibrosis score. E, Representative image of EE biopsy stain
Pediatric patients with EE have increased subepithelial fibrosis and TGF-β1. A-D, Trichrome stain of normal, GERD, EE esophageal biopsies and fibrosis score. E, Representative image of EE biopsy stained for TGF-β1 (red; inset shows green nucleus). F, Quantitated TGF-β1–positive cells in normal patients, patients with GERD, and patients with EE. G-I, Eosinophils express MBP (red), TGF-β1 (green), or both (yellow). ∗∗P < .005.
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Increased nuclear phosopho-SMAD2/3 in the esophagus of patients with EE. A-F, Representative image of phospho-SMAD2/3 staining in epithelial (EPI) and lamina propria cells in patients with GERD (arrowIncreased nuclear phosopho-SMAD2/3 in the esophagus of patients with EE. A-F, Representative image of phospho-SMAD2/3 staining in epithelial (EPI) and lamina propria cells in patients with GERD (arrows show phopho-SMAD2/3–negative nuclei) and patients with EE. G-I, A subset of actively proliferating epithelial cells coexpress (yellow) MIB-1 (green) and phosopho-SMAD2/3 (red). J, Quantitation of phospho-SMAD2/3–positive cells in normal, GERD, and EE. ∗P < .05; ∗∗P < .005.
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Increased vascularity and VCAM-1 in the subepithelial esophagus of patients with EE. A-C, Representative images of vWF-positive vessels in the lamina propria of normal patients, patients with GERD, anIncreased vascularity and VCAM-1 in the subepithelial esophagus of patients with EE. A-C, Representative images of vWF-positive vessels in the lamina propria of normal patients, patients with GERD, and patients with EE (inset shows blue nuclei). D and E, Quantitation of vWF and VCAM-positive vessels. ∗P < .05; ∗∗P < .005.
Supported by the American Academy of Allergy, Asthma & Immunology Education and Research Trust (ERT) Clinical Research Grant (S.S.A.), National Institutes of Health T32 Training award AI 007469 (S.S.A.), and National Institutes of Health grant AI 38425 (D.H.B.).Disclosure of potential conflict of interest: S. S. Aceves has received grant support from the American Academy of Allergy, Asthma and Immunology Clinical ERT. D. H. Broide has received grant support from the National Institutes of Health. The other authors have declared that they have no conflict of interest.
PII: S0091-6749(06)02136-1
doi: 10.1016/j.jaci.2006.10.016
© 2007 American Academy of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.
« Previous
Next »
The Journal of Allergy and Clinical Immunology
Volume 119, Issue 1
, Pages
206-212
, January 2007
