Abstract Accepted

Preliminary data from our Eosinophilic Esophagitis research study has been accepted as an abstract poster presentation. The abstract, Gene Expression Profile of Inflammatory Mediators and Extracellular Matrix and Adhesion Molecules in Eosinophilic Esophagitis (781818,) will be presented during Digestive Disease Week, to be held at the Ernest N. Morial Convention Center in New Orleans, LA, May 1 - May 5, 2010. A copy of the abstract is below:


Eosinophilic esophagitis (EoE) is a disease of the esophagus of increasing prevalence, encountered in children and adults. It is an inflammation of the esophagus, presumed to be of allergic origin, causing linear furrows and thin crepe-like mucosa. EoE does not respond to acid suppression therapy and can lead to dysphagia and esophageal strictures. Microscopic observation reveals massive eosinophil infiltration, remodeling of the esophageal epithelium, severe basal cells hyperplasia and subepithelial fibrosis. Our aim is to investigate the cellular and molecular factors involved in esophageal tissue damage and remodeling.

We used real-time qPCR to study the expression of two panels of genes in pinch biopsies obtained during routine endoscopy procedures in EoE and normal pediatric patients (NL). The first panel contains 84 genes involved in the inflammatory response. The second panel contains 84 genes playing a role in extracellular matrix (ECM) structure, cell-to-cell communications and cell-matrix adhesion. We also used cytokines and growth factors protein arrays as well as immunohistochemistry (IHC) to determine and localize specific proteins involved in the above pathways.

The inflammation gene array data show that eotaxin 3 and its receptor CCR3 are very prominently upregulated (~200 folds) and (~23 folds) respectively. Interleukins (IL), IL13 and IL5 are upregulated by ~10 and ~4 folds respectively. These data are consistent with previously reported observations. In the ECM gene panel, CD44 and CD54 (ICAM1), both hyaluronan binding molecules, and genes for ECM proteases (ADAMTS1 and MMP14) are upregulated significantly. Collagen genes (COL6A1 and COL15A1) are upregulated (~3 folds), whereas COL14A1 is downregulated (~2 folds). IHC experiments using an antibody to CD44 showed more intense staining in EoE biopsies than in NL. A label-based cytokine and growth factors antibody array showed an increase in epidermal growth factor (EGF) and fibroblast growth factor (FGF7) in EoE biopsies.

We have identified a number of novel genes whose expression is altered in EoE. Further investigating their role in inflammation and esophageal tissue damage could reveal the mechanisms of remodeling observed in the disease.

Abdulnour-Nakhoul, Solange M.; Al-Tawil, Youhanna S.; Eidelwein, Alexandra P.; Noel, R. Adam; Hansen, Molly; Gyftopoulos, Alex A.; Butcher, Kathy F.; Brown, Karen L.; Nakhoul, Nazih.

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