Overall, although the possible role for LCN2 in IPF pathogenesis remains obscure, the acute increase in Lcn2 expression following both LPS-induced ALI and BLM-induced pulmonary inflammation and fibrosis suggests that Lcn2 is an acute phase protein of lung damage in mice, as previously suggested for acute kidney injury (9) and acute exacerbation of cystic fibrosis (52), correlating with epithelial damage and neutrophilic infiltration. Here, LCN2 is linked to idiopathic pulmonary fibrosis.