Coordinate interaction between IL-13 and epithelial differentiation cluster genes in eosinophilic esophagitis1

We have previously proposed that the pathogenesis of eosinophilic esophagitis (EE) is mediated by an IL-13–driven epithelial cell response associated with marked gene dysregulation including eotaxin-3 overproduction. Herein, we compared epithelial responses between normal (NL) and EE patients aiming...

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Bibliographic Details
Published in:The Journal of immunology (1950) 2010-03, Vol.184 (7)
Main Authors: Blanchard, Carine, Stucke, Emily M., Burwinkel, Karen, Caldwell, Julie M., Collins, Margaret H., Ahrens, Annette, Buckmeier, Bridget K., Jameson, Sean C., Greenberg, Allison, Kaul, Ajay, Franciosi, James P., Kushner, Jonathan P., Martin, Lisa J., Putnam, Philip E., Abonia, J. Pablo, Wells, Suzanne I., Rothenberg, Marc E.
Format: Article
Language:English
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Summary:We have previously proposed that the pathogenesis of eosinophilic esophagitis (EE) is mediated by an IL-13–driven epithelial cell response associated with marked gene dysregulation including eotaxin-3 overproduction. Herein, we compared epithelial responses between normal (NL) and EE patients aiming to uncover molecular explanations for EE pathogenesis. Esophageal epithelial cells could be maintained up to 5 passages, with 67% and 62% of cell lines reaching confluence in NL and EE, respectively. Both sets of epithelial cells avidly responded to IL-13 at similar levels as assessed by eotaxin-3 production. Acidic pH increased cellular release of eotaxin-3 (4.6 ± 1.98 ng/mL vs. 12.46 ± 2.90 ng/mL at pH 7.4 and 4 respectively, p
ISSN:0022-1767
1550-6606
DOI:10.4049/jimmunol.0903069