Hepatic fibrosis is examined in mice infected with schistosome species pathogenic for man. Mouse strains developed markedly different degrees of hepatic fibrosis following infection with S. mansoni. T cells are important for the formation of granulomas in both S. mansoni and S. japonicum infected mice, as determined from examination of athymic and B cell depleted mice. Current studies are focused on determining which subsets of T cells are involved in regulation of S. japonicum egg granulomas. BALB/c mice are not much more responsive to S. japonicum eggs than are BALB/c nu/nu mice, precluding studies of cell transfer in this strain. BALB/c mice do have more fibrosis than do their nude couterparts, emphasizing the role of T cells in hepatic fibrosis in this system and providing one more example of the dissociation of granuloma size and fibrosis. T cells are required for the formation of normal granulomas, as indicated by marked differences between NCR outbred nu/nu versus nu/+ and between C57BL/6 nu/nu versus C57BL/6. Studies of cell transfer from normal into nude mice have begun with this last combination. The intensity of murine S. mansoni infection was found to modulate hepatic pathology. With increasing intensity of infection a smaller proportion of eggs was found in the liver and less fibrosis per egg was noted. The volume of hepatic granulomas, in contrast to S. japonicum infected mice, did not vary with infection intensity. The dissociation of the effects of infection intensity on fibrosis and granuloma volume indicates that they are under different regulatory influences. The fecundity of S. mansoni worm pairs decreased with increasing intensity of infection, again in contrast to S. japonicum infected mice.
