Pro-inflammatory mediators modulate endoplasmic reticulum (ER) stress, defined as alterations in ER homeostasis under various stress. As a bacterial endotoxin, lipopolysaccharide (LPS) is involved in numerous inflammatory diseases, and IL-17 has been known to be implicated in LPS-induced lung inflammation. However, it is not known exactly how IL-17 interacts with ER stress in LPS-related lung inflammation. In this study, using a murine model of LPS-induced lung inflammation, effects of IL-17 inhibition using anti-IL-17 antibody on LPS-induced lung inflammation were examined, especially in relation to ER stress. Inhibition of IL-17 reduced significantly LPS-induced increases of GRP78 and CHOP protein levels in lung tissues. IL-17 inhibition also lowered LPS-induced increases of unfolded protein response (UPR)-related markers in the lung. Furthermore, increases of airway inflammatory cell infiltrations, vascular leakages, and various pro-inflammatory mediators after LPS treatment were decreased by the neutralization of IL-17. Moreover, administration of 4-phenylbutyrate (PBA), an ER stress inhibitor, attenuated pathologic features as well as increases of various ER stress markers of LPS-induced lung inflammation. And, increases in nuclear translocation of NF-κB p65, expression of Toll-like receptor4 (TLR4), and infiltration of dendritic cells (DCs) into lungs after LPS treatment were reduced after IL-17 blockade. Our results suggest that IL-17 inhibition improves LPS-induced lung inflammation partly through the modulation of ER stress.