Abstract Human matrix metalloproteinase-1 (MMP-1) has been shown to contribute to the regression of experimental liver fibrosis when ectopically expressed in rodents. It remains unknown whether the same mechanism exists in chronic liver diseases in humans. This study was conducted to elucidate the functional contribution of MMP-1 to the pathophysiology of nonalcoholic steatohepatitis (NASH). Samples from 19 histologically proven NASH patients were examined together with normal liver specimens from four subjects. Expression of MMP-1, caveolin-1, active and latent forms of TGF-β, and type 1 procollagen was analyzed using immunohistochemical, western blotting and immunoelectron microscopic (IEM) examinations. In the early stage of NASH, MMP-1 was expressed predominantly in Kupffer cells and monocytes. Remarkable expression of MMP-1 and caveolin-1 was observed in hepatic progenitor cells (HPCs), hepatic stellate cells (HSC) and proliferating capillary endothelial cells in the advanced stage of NASH. MMP-1 immunostaining was significantly greater in advanced (p < 0.014) and early (p < 0.016) NASH than in control. IEM revealed MMP-1-immunoreactive products in HPCs/HSC/small hepatocytes. Active form of TGF-β and type I procollagen were detected at the edge of those capillary endothelial cells adjacent to the HPCs. MMP-1 expressed in HPCs/small hepatocytes/ capillary endothelial cells may contribute, at least in part, to the repair and regeneration of fibrotic liver through the caveolin-1 signal in the advanced stage of NASH.
Keywords: MMP-1; TGF-β caveolin-1; nonalcoholic steatohepatitis; hepatic progenitor cells; spatiotemporal expression

Abstract Talc induced pulmonary granulomatosis is a known pulmonary condition that is associated with intravenous drug exposure. Only one documented case of talc induced pulmonary granulomatosis in a patient with cystic fibrosis (CF) has been reported in the literature. We add another case of such condition. Our goal is to increase the awareness of this under recognized potential cause of CF related pulmonary induced fibrosis and hypertension. Patients with risk factors and with findings similar to the reported patient may benefit from further clinical and pathological evaluation for talc induced pulmonary granulomatosis.
Keywords: talc induced pulmonary granulomatosis; talcosis; cystic fibrosis