Animal models currently used to study IPF do not appropriately mimic the morphologic changes of IPF. As stated in the National Heart, Lung, and Blood Institute workshop summary,2 persistent progressive fibrosis with evidence of temporal heterogeneity is a hallmark of IPF; these features are lacking in the contemporary models of lung fibrosis. Currently, the primary model for the study of IPF is the bleomycin-treated rodent; however, neither the acute nor chronic pulmonary changes resemble UIP. Administration of bleomycin to mice, rats, and hamsters results in pulmonary inflammation and fibrogenesis. Neither the acute or chronic morphology of the lungs of bleomycin-treated rats resembles the changes of IPF. Indeed, there is evidence of spontaneous resolution of the lung injury 4 months after bleomycin treatment, a phenomenon that is not seen in IPF. www.xalatan-eye-drops.com
Because the cause(s) and pathogenesis of IPF are not well understood in humans, the identification of an animal in which pulmonary disease spontaneously develops that mimics both the clinical progression and morphologic features of human IPF has important implications in the study of the human disease. Spontaneous IPF in another species provides an opportunity to investigate common cellular and biochemical features between the two species. Confirming the presence, morphology, and distribution of cellular effectors presumed to be important in the human disease (ie, myofibroblasts and type II pneumocytes) in another species with IPF further suggests their importance in maintaining the lung phenotype. In light of the limitations of the currently utilized animal models of IPF, identification of spontaneous IPF in an animal that shares the morphologic fidelity with the human disease is the first step in establishing a true model of the disease.