Pharmacological inhibition with SB203580 significantly reduced the permeability, the lung fibrosis staining of collagen and fibroblasts, the phosphorylation of P38, and MIP-2 production, but not IP-10 production – suggesting that P38 played a less significant role than the Akt–ERK1/2 pathway in the mechanism of high-tidal-volume-induced pulmonary fibrosis. Here, CXCL10 is linked to pulmonary fibrosis.