IL-17 appears to act rapidly as an innate immune responder during infection, before the onset of a classic role of IL-17 through adaptive T cell response. In addition, IL-17 is implicated in lipopolysaccharide (LPS)-induced lung inflammation, in which ER stress has been known to play a pivotal role pathophysiologically. In this study, to elucidate the role of IL-17A in LPS-induced lung inflammation focusing on the link with ER stress in a mouse model of LPS-induced lung injury, we treated the mice with IL-17A neutralizing antibodies and 4-PBA, a representative ER stress regulator. In addition, we evaluated the effects of IL-17A on ER stress induced in LPS-stimulated bronchial epithelial cells. Our result showed that inhibition of IL-17A diminished the typical features of lung injury including pulmonary neutrophilia and vascular leakage and the increased ER stress and improves LPS-induced lung inflammation. Moreover, 4-PBA also attenuates the LPS-induced lung inflammation and the expression of IL-17A. Intriguingly, the expression of IL-17A was observed in LPS-stimulated airway epithelial cells and IL-17A can induce the enhancement of ER stress and NF-κB activation in airway epithelial cells. Lastly, our results also showed that increases in nuclear translocation of NF-κB, infiltration of DCs into lungs, and TLR4 expression after LPS treatment were significantly reduced by the inhibition of IL-17A in the lung. This study indicates that the relationship between IL-17 and ER stress plays an important role in the pathogenesis of LPS-induced inflammation. IL-17 appears to act rapidly as an innate immune responder during infection, before the onset of a classic role of IL-17 through adaptive T cell response. In addition, IL-17 is implicated in lipopolysaccharide (LPS)-induced lung inflammation, in which ER stress has been known to play a pivotal role pathophysiologically. In this study, to elucidate the role of IL-17A in LPS-induced lung inflammation focusing on the link with ER stress in a mouse model of LPS-induced lung injury, we treated the mice with IL-17A neutralizing antibodies and 4-PBA, a representative ER stress regulator. In addition, we evaluated the effects of IL-17A on ER stress induced in LPS-stimulated bronchial epithelial cells. Our result showed that inhibition of IL-17A diminished the typical features of lung injury including pulmonary neutrophilia and vascular leakage and the increased ER stress and improves LPS-induced lung inflammation. Moreover, 4-PBA also attenuates the LPS-induced lung inflammation and the expression of IL-17A. Intriguingly, the expression of IL-17A was observed in LPS-stimulated airway epithelial cells and IL-17A can induce the enhancement of ER stress and NF-κB activation in airway epithelial cells. Lastly, our results also showed that increases in nuclear translocation of NF-κB, infiltration of DCs into lungs, and TLR4 expression after LPS treatment were significantly reduced by the inhibition of IL-17A in the lung. This study indicates that the relationship between IL-17 and ER stress plays an important role in the pathogenesis of LPS-induced inflammation.