The aim of this study is to test the hypothesis that the early changes in lung mechanics and the amount of type III collagen fiber do not predict the evolution of lung parenchyma remodeling in pulmonary and extrapulmonary acute lung injury (ALI). For this purpose, we analyzed the time course of lung parenchyma remodeling in murine models of pulmonary and extrapulmonary acute lung injury with similar degrees of mechanical compromise at the early phase of ALI. Lung histology (light and electron microscopy), the amount of elastic and collagen fibers in the alveolar septa, the expression of matrix metalloproteinase (MMP)-9, and mechanical parameters (lung resistive and viscoelastic pressures, and static elastance) were analyzed 24 hours, 1, 3, and 8 weeks after the induction of lung injury. In control (C) pulmonary (p) and extrapulmonary (exp) groups saline was intratracheally (i.t., 0.05 ml) instilled and intraperitoneally (i.p., 0.5 ml) injected, respectively. In ALIp and ALIexp groups, mice received E. coli lipopolysaccharide (10 µg, i.t. and 125 µg, i.p., respectively). At 24 h all mechanical and morphometrical parameters, as well as type III collagen fiber content increased similarly in ALIp and ALIexp groups. In ALIexp, all mechanical and histological data returned to control values at 1 week. However, in ALIp static elastance returned to control values at 3 weeks, while resistive and viscoelastic pressures, as well as type III collagen fibers and elastin remained elevated until the 8^th week. ALIp showed higher expression of MMP-9 than ALIexp. In conclusion, insult in pulmonary epithelium yielded fibroelastogenesis, while mice with ALI induced by endothelial lesion developed only fibrosis that was repaired early in the course of lung injury. Furthermore, early functional and morphological changes did not predict lung parenchyma remodeling.