Molecular and cellular basis of hepatic fibrogenesis in experimental schistosomiasis mansoni infection

Memórias do Instituto Oswaldo Cruz

David J. Wyler¹ 

[1] ,New England Medical Center Hospitals Department of Medicine Division of Geographic Medicine and Infectious DiseasesBoston,USA

关键词: schistosomiasis;    hepatic fibrogenesis;   

DOI  :  10.1590/S0074-02761992000800017

来源: SciELO

【 摘 要 】

Morbidity in schistosomiasis mansoni occurs primaryly as a result of the complications of hepatic fibrosis. Yet, the pathogenesis of schistosomal hepatic fibrosis is poorly understood. The fact that hepatic egg granuloma is the hallmark of this infection suggests a potential role for granulomatous inflamation in hepatic fibrogenesis. Our studies in a murine schistosomiasis model indicate that hepatic granuloma cells secrete a variety of fibrogenic cytokines that may initiate the scarring process. Among these cytokines, we identified a novel protein that we designated fibroplast stimulating factor-1 (FsF-1). FsF-1 is a lymphokine that can stimulate fibroplast growth and matrix synthesis. A notable feature of hepatic fibrosis in this model is that production of FsF-1 and other granuloma-derived fibrogenic cytokines is down-regulated in chronic infection, an event that may be under immunological control. The spontaneous reduction of FsF-1 secretion presumably accounts for reduced scar formation late in infection of mice. In the context of relevant clinical studies, our findings engender the hypothesis that Symmer's fibrosis may develop in a small suppopulation of individuals as a result of immunogenetically-determined dysregulation of fibrogenic cytokine production.

【 授权许可】

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