Transient receptor potential ankyrin 1 (TRPA1) is known as one of the nociceptors expressed in sensory neurons. It also plays a role in non-neural cells in inflammatory sites. However, the regulatory mechanisms for the reactivity of TRPA1 in these cells under inflammatory conditions are not clear. To clarify these mechanisms, we examined the effects of inflammatory cytokines (interleukin [IL]-1 alpha, IL-1 beta and tumor necrosis factor alpha [TNF alpha]) on TRPA1 reactivity and expression in the endogenously TRPA1-expressing lung tumor cell line A549. Treatment with IL-l alpha, but not IL-1 beta or TNF alpha, increased the number of cells responding to allyl isothiocyanate, a TRPA1 agonist, in a dose- and time-dependent-manner. The IL-l alpha-induced increase of TRPA1 responsiveness was inhibited by an extracellular-regulated kinase (Erk) inhibitor (PD98059) but not by inhibitors of c-Jun kinase, p38 mitogen-activated protein kinase or phosphatidylinositol-3 kinase. Phosphorylation of Erk gradually increased at 24 h after its transient induction in cells treated with IL-l alpha. IL-l alpha increased the TRPA1 levels on biotinylated cell surface proteins. These results suggest that IL-1 alpha enhances the translocation of TRPA1 to the plasma membrane via the activation of Erk in A549. TRPA1 may have a pathophysiological role in. non-neural lung cells under inflammatory conditions. (C) 2017 Elsevier Inc. All rights reserved.