Expression of TARC in Nasal Epithelial Cells by IL-4/IL-13 and TNF-alpha in Allergic Rhinitis

ABSTRACT

BACKGROUND: Thymus and Activation-Regulated Chemokine (TARC) is a highly specific ligand for CCR4 expressed in Th2 lymphocytes. Local production of TARC may play an important role in the induction and maintenance of allergic inflammation with the infiltration of Th2 lymphocytes. However, the cellular sources of TARC among patients with allergic rhinitis (AR) remain unclear. OBJECTIVE: We investigated that nasal epithelial cells from AR could produce TARC and that they could produce TARC differently by various stimulation of cytokines. METHODS: Inferior turbinate mucosal tissues were collected from six patients with AR sensitized to house dust mite. Nasal epithelial cells were isolated, cultured and stimulated with IL-4, IL-13 or TNF-a alone or in combination. The level of TARC in the supernatant was measured by ELISA and mRNA expression of that in the cells by RT-PCR. RESULTS: The level of TARC from cultured nasal epithelial cells (CNEC) among allergic rhinitis patients was higher than that in the control group. IL-4 or IL-13 or TNF-a alone did not upregulate TARC production from CNEC. However, Th2 cytokines in combination with TNF-a increased the production of TARC in CNEC. CONCLUSION: IL-4, IL-13 and TNF-a could upregulate TARC production from nasal epithelial cells in allergic rhinitis and contribute to the infiltration of Th2 cells to the tissue during allergic inflammation.