Idiopathic pulmonary fibrosis (IPF) affects 200 000 patients in the United States of America. IPF is responsible for changes in the micro-architecture of the lung parenchyma, such as thickening of the alveolar walls, which reduces compliance and elasticity. In this study, we verify the hypothesis that changes in the microarchitecture of the lung parenchyma can be characterized by exploiting multiple scattering of ultrasound waves by the alveolar structure. Ultrasound propagation in a highly scattering regime follows a diffusion process, which can be characterized using the diffusion constant. We hypothesize that in a fibrotic lung, the thickening of the alveolar wall reduces the amount of air (compared with a healthy lung), thereby minimizing the scattering events. Pulmonary fibrosis is created in Sprague-Dawley rats by instilling bleomycin into the airway. The rats are studied within 3 weeks after bleomycin administration. Using a 128-element linear array transducer operating at 7.8 MHz, in vivo experimental data are obtained from Sprague-Dawley rats and the transport mean free path (L*) and backscatter frequency shift (BFS) are evaluated. Significant differences ( ) in the L* values between control and fibrotic rats and in the BFS values between fibrotic and edematous rats showcase the potential of these parameters for diagnosis and monitoring of IPF.