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Identification of Spontaneous Feline Idiopathic Pulmonary Fibrosis: UIP changes

Identification of Spontaneous Feline Idiopathic Pulmonary Fibrosis: UIP changesCats with IPF acquire lung histopathology similar to human IPF. Previous to the 2000 statement designating UIP as the pathologic manifestation of IPF, acute interstitial pneumonia, desquamative interstitial pneumonia, and NSIP were also considered variations of IPF. These other pulmonary diseases lack the temporal heterogeneity and evidence of ongoing fibrogenesis of IPF. Complicating this classification system is the finding of Flaherty et al, who found considerable variation between lobes of individual patients with IPF; many of the patients had histologic features consistent with fibrotic NSIP in lobes away from the UIP changes. We are unable at this time to discuss the uniformity of changes between lobes in individual cats because the tissues examined represent material collected from individual lobes, prior to knowledge of the nature of the disease process and the potential for interlobar variability. Examination of entire lung fields from affected cats, with careful sampling of a variety of lobes, will be important to address this question. this

Microscopic honeycomb change is very common, and characteristic in human and feline IPF. The identification of this morphologic feature, which is not a feature of rodent models of lung fibrosis, has important implications for studying the disease. Numerous important growth factors, including many with profibrogenic activity such as transforming growth factor-^, can be immunohistochemically localized to this population of cells in humans. Studies are ongoing to immunohistochemically characterize the presence of similar proteins in the feline lung. Mucous cell metaplasia in feline IPF is similar to reports in honeycomb lung of humans.- The mucous metaplasia in feline and human IPF may be an adaptive response to the chronic, progressive injury to the lung. Alternatively, this phenotype may reflect local production of cytokines, such as interleukin-13, which are known to induce pulmonary mucous cell metaplasia. The role of mucous cell metaplasia in the progression of the disease is unclear, although excess mucus production has been associated with a poorer prognosis in human patients with IPF.