This study describes spontaneous feline IPF, a newly identified chronic lung disease of domestic cats that shares critical features with human IPF. The important gross pathology, histopa-thology, cell differentiation markers, and ultrastruc-tural features are compared to the well-described features of the disease in humans. IPF in humans is a chronic respiratory disease whose pathology is characterized by temporally heterogeneous, persistent, progressive fibrosis of the lung, usually without significant inflammation. The characteristic morphology consists of patchy remodeling in the lungs leading to honeycomb lung late in the disease, with the characteristic histopathology. This histopathol-ogy shows evidence of temporal heterogeneity with fibrosis, fibroblast foci, and evidence of honeycombing in the parenchyma. Each of these features is found in spontaneous feline IPF. Additionally, ultra-structural features of the type II pneumocytes in feline IPF share morphologic features with the type II cells in a familial form of human UIP, suggesting that the disease in cats may be due to an abnormality in the type II cell. Genetic analysis of surfactant protein genes in affected and normal cats is currently underway, providing hope that the domestic cat may be developed as a new model of IPF. fml ophthalmic drops
The gross lesions within the lungs of feline IPF share similarities with human IPF. The lungs of human patients at autopsy are typical of end-stage interstitial lung disease with fibrosis and honeycombing of the alveolar parenchyma. In both feline and human IPF, the distribution of the lesions is patchy, with normal areas of lung interspersed with adjacent foci of fibrosis and honeycomb change; this distribution is considered important in the diagnosis of IPF. Unlike humans, where honeycomb lung is apparent as greatly dilated peripheral air spaces, the honeycomb change in the feline lung is comprised of smaller microhoneycombing, and only occasionally forms the typical lesions of human IPF. There are no detailed reports of the gross pathology in rodent models of IPF that share the features of the human and feline disease. Because of the size of the feline lung relative to rodents, and the discrete nature of the diseased vs more normal lung, feline IPF can facilitate investigations into microenvironmental changes within the IPF lung that are important in the pathogenesis of the disease. Work is currently underway to investigate differences in the fibroblast/ myofibroblasts populations from fibrotic and nonfi-brotic feline lung; similar work has been accomplished in human IPF lung.