Expression of toll-like receptors 2 and 3 on esophageal epithelial cell lines and on eosinophils during esophagitis.

BACKGROUND: 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. AIMS: 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.
METHODS: 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.
RESULTS: 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.
CONCLUSIONS: 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.