A study of idopathic interstitial pneumonia with transgenic mouse (HCV)

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Pathogenesis of IPF (interstitial pulmonary fibrosis) is still unclear despite of its poor prognosis. We hypothesized that HCV, which has been recognized, as one of major pathogen of fibrous change in liver, may play a role in IIP. First, we confirmed patients with IPF have antibody against HCV in a larger population and are more frequently positive in RT-PCR to HCV as compared to controls. In this study we investigated the role of this virus in IPF using the HCV transgenic mouse. In HCV transgenic mouse significantly sever fibrous changes were observed in lung with a small amount of silica such as 8 mg. Pro-inflammatory cytokines such as IGF-1 and TGF-beta increased in the lung in response to silica in a dose dependent manner but no significant differences were observed between transgenic and non-transgenic mouse. On the other hand, HCV transgenic mouse had significantly high expression of mRNA of IL-4 and INF-gamma as compared to controls. These findings proposed that HCV might promote the progression of fibrous changes in lung in response to silica with different profiles of cytokines.