miR-143 inhibits interleukin-13-induced inflammatory cytokine and mucus production in nasal epithelial cells from allergic rhinitis patients by targeting IL13Rα1

• miR-143 inhibits GM-CSF, eotaxin and MUC5AC production in IL-13-stimulated NECs.
• miR-143 directly targets and suppresses IL13Rα1 expression.
• The IL13Rα1 pathway may be a potential target for control of AR by miR-143.

Allergic rhinitis (AR) is a common chronic inflammatory condition of the nasal mucosal tissue. The interleukin-13 (IL-13) signaling pathway is of great importance in the pathogenesis of AR. However, how the signaling molecules in this pathway are regulated, particularly through microRNAs (miRNAs), remains unclear. In the present study, we investigated the regulatory role and mechanism of miRNA-143 (miR-143) in IL-13-induced inflammatory cytokine and mucus production in nasal epithelial cells (NECs) from AR patients. Our results showed that forced expression of miR-143 significantly decreased the mRNA and protein expression levels of granulocyte–macrophage colony-stimulating factor (GM-CSF), eotaxin and mucin 5AC (MUC5AC) in IL-13-stimulated NECs. Moreover, we confirmed that miR-143 directly targeted and significantly suppressed IL-13 receptor α1 chain (IL13Rα1) gene expression. This study thus suggests that miR-143 regulation of IL-13-induced inflammatory cytokine and mucus production in NECs from AR patients probably partly depends on inhibition of IL13Rα1. Therefore, the IL13Rα1 signaling pathway may be a potential target for the prevention and treatment of AR by miR-143.

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