Expression of Toll-Like Receptors 2 and 3 on Esophageal Epithelial Cell Lines and on Eosinophils During Esophagitis

The chronic disease eosinophilic esophagitis may be mediated by the innate immune system. Activation of toll-like receptors (TLRs) in other tissues is known to initiate eosinophil infiltration, thus TLRs may be a potential mediator of esophageal eosinophilia. Little is known about TLRs in the esophagus. The purpose of this study was to identify the presence and activation of TLR2 and TLR3 on esophageal epithelial cell lines, primary epithelial cells and mucosal esophageal biopsies. TLR2 and TLR3 were identified by immunocytochemistry and immunoblot. PCR assessed alterations to gene expression by activation of TLR2 and TLR3. Immunohistochemistry co-localized eosinophils and TLR2/TLR3 on esophageal biopsies. TLR2 and TLR3 were expressed on the esophageal adenocarcinoma cell lines TE-1 and TE-7, but only TLR3 was present on the esophageal epithelial cell line HET-1A. Thymic stromal lymphopoietin gene expression was altered in response to ligands zymosan and polyI:C, demonstrating activation. Primary esophageal epithelial cells did not express TLR2 or TLR3. In esophageal biopsies, TLR2 and TLR3 expression was limited to eosinophils and other immune cells during esophagitis. TLR2 and TLR3 expression on cultured esophageal epithelial cells differs from TLR2 and TLR3 expression in esophageal biopsies, which is limited to immune cells during esophagitis.