Schistosomes, fibroblasts, and growth factors: how a worm causes liver scarring

The traditional concept of tissue scarring as a static pathological endpoint has been replaced by the modern perspective of a potentially reversible process comprising a sequence of discrete biological events (cell recruitment and hyperplasia, excessive matrix production, and matrix degradation). Cytokines, including several produced by inflammatory cells, have been identified that specifically regulate these events. Research into the cellular and molecular biology of scar formation is motivated by clinical and basic scientific considerations. One model of fibrogenesis that is being studied in detail is the liver fibrosis associated with schistosomiasis. In this helminthic infection, the host's granulomatous inflammatory response to the parasite eggs apparently lead to scar formation. A novel lymphokine that is mitogenic for fibroblasts and is produced by CD4+ lymphocytes in the granuloma has been found in infected livers. Preliminary evidence for the existence of immunoregulatory mechanisms of fibrogenesis in this disease also has been obtained. The potential role of genetic determinants that may influence this process needs to be further studied.