Inhibition of IL-32 signaling by bamboo salt decreases pro-inflammatory responses in cellular models of allergic rhinitis.

Previously, we showed the antiallergic effect of bamboo salt (BS) in allergic rhinitis (AR). We also demonstrated that interleukin (IL)-32 is an important mediator of AR. The aim of this study was to evaluate the effect and specific underlying mechanism of BS, NaCl, and the mineral mixture (components of BS other than NaCl, including zinc, magnesium, and potassium, Mix) on IL-32 signaling using the human monocyte cell line, THP-1. Here, we documented for the first time that BS significantly decreased IL-32-induced thymic stromal lymphopoietin protein and mRNA expression in THP-1 cells. BS treatment significantly inhibited IL-32-induced proinflammatory cytokine production including IL-1ß, IL-8, and tumor necrosis factor (TNF)-α by suppressing nuclear factor-κB, p38 mitogen-activated kinase, and caspase-1 pathways. The presence of BS or Mix effectively suppressed IL-32-induced macrophage-like cell differentiation but NaCl exhibited no effect on monocyte-to-macrophage-like cell differentiation. In IL-32-induced macrophages, the production of IL-1ß, IL-6, IL-8, and TNF-α, and expression of inducible nitric oxide synthase and cyclooxygenase-2, induced by lipopolysaccharide was dramatically decreased in a dose-dependent manner after BS treatment. BS also significantly decreased IL-32-induced nitric oxide, IL-8, and TNF-α production. Furthermore, BS inhibited granulocyte-macrophage colony-stimulating factor-induced IL-32 and IL-8 protein and mRNA expression in EOL-1 cells. Taken together, BS suppressed inflammatory activity by inhibiting the IL-32 signaling pathway in AR.