Morbidity in schistosomiasis is caused by the host response to schistosome eggs deposited in the venous system and carried to the tissues. Pathology is proportional to the number of eggs laid. It is thus important to understand factors underlying worm fecundity and the extent to which fecundity is reflected by eggs passed in the feces, the measurable indicator of infection intensity in humans. Treatment of mice with anti-TNF-alpha resulted in slightly smaller circumoval granulomas and slightly decreased egg laying in S. mansoni but not S. japonicum infections. Antibodies to TGFbeta, IL-1O or IL-6 in S. mansoni infected mice did not affect worm fecundity. Egg laying was also normal in S. mansoni-infected CD8+ and IL-1O knockout mice.
