The course of Toxoplasma gondii infection was studied in IL-4-deficien
t mice from three genetic backgrounds and their wild-type counterparts
following peroral inoculation of tissue cysts. Survival rates were si
gnificantly reduced in disease-susceptible C57 BL/6 mice and Fl (C57BL
/6 x 129Sv) mice deficient in IL-4 compared with wild-type controls. I
n contrast, this difference was not observed in T. gondii-resistant BA
LB/c mice. However, brain tissue cyst burdens in IL-4-deficient mice w
ere either equivalent to (C57BL/6 and BALB/c mice) or significantly le
ss (B6/129 mice) than similarly infected wild-type mice. Thus strain-s
pecific differences in the course of T. gondii were demonstrated in th
e absence of IL-4. The course of T. gondii infection was also compared
between B6/129 IL-4-deficient mice and their wildtype counterparts fo
llowing peroral challenge with 20 tissue cysts on day 12 of pregnancy.
Age-matched non-pregnant IL-4-/- and IL-4+/+ mice were also infected
to assess the role of IL-4 on T. gondii infection during pregnancy. Di
sease phenotypes, as measured by mortality, were reversed if infection
s were initiated during pregnancy compared with non-pregnant infection
. Thus significant mortality occurred immediately post partum in IL-4/+ mothers, while all IL-4-/- mothers survived. Cyst burdens 28 days p
.i. were significantly lower in IL-4-/- mothers than IL-4+/+ mothers a
nd both IL-4-/- and IL-4+/+ non-pregnant mice. Congenital disease tran
smission as measured by foetal death or vertical disease transmission
was independent of the presence or absence of IL-4. These studies demo
nstrate a role for IL-4 in pregnancy-induced immunosuppression and the
associated increased susceptibility to T. gondii infection. (C) 1998
Australian Society for Parasitology. Published by Elsevier Science Ltd
.