Abstract
Schistosoma mansoni-infected mice were administered at the time of parasite residency in the lung with recombinant murine interleukin (IL)-2 or interferon-gamma (IFN-γ), to evaluate the impact of cytokines in host responses to primary schistosomiasis.
S. mansoni lung-stage schistosomula did not affect plasma lipids levels in BALB/c, while elicited significant (
p
<
0.05) increase in free fatty acids (FA) and decrease in cholesterol plasma levels in C57BL/6 and CD1 mice, and stimulated expression of mRNA for Th2 cytokines in BALB/c and Th1 cytokines in C57BL/6 and CD1 mice. Production of specific antibodies was negligible in the 3 strains. Interleukin-2 treatment elicited significant (
p
<
0.001) decrease in triglycerides (TG) in CD1, and decrease in TG and cholesterol plasma levels and down-regulation of TNF-α mRNA expression in C57BL/6 mice. Induction of type 2 cytokines and/or IFN-γ mRNA expression did not lead to increase in percentage of specific antibody responders in any mouse strain. Exogenous IL-2-related reduction in cholesterol plasma levels and TNF-α mRNA expression in C57BL/6 mice was associated with significant (
p
<
0.05) decrease in adult worm recovery and egg count. Treatment with IFN-γ elicited significant (
p
<
0.05) free FA plasma levels increase in BALB/c and C57BL/6 and decrease in CD1 mice. Expression of type 2 cytokines mRNA was stimulated in BALB/c and CD1 mice, yet was not accompanied with increase in humoral responses. Exogenous IFN-γ-related reduction in free FA plasma levels and IFN-γ mRNA response, and up-regulation of TNF-α mRNA expression in CD1 mice were associated with significant increase in adult worm burden and egg load. The data were discussed in an attempt to define host factors predictive of resistance to schistosome infection.