Challenge worm survival was significantly reduced when BALB/cByJ mice
were vaccinated against Strongyloides stercoralis infective third stag
e larvae (L3) regardless of whether the challenge infections consisted
of systemically migrating L3 or L3 implanted in diffusion chambers. T
he only cell type that increased in number in diffusion chambers in im
munized mice, 1 week after booster immunizations, was the eosinophil,
and maximal levels of eosinophils were coincident with parasite killin
g. Mice were treated with mAb to eliminate IL-5 or granulocytes to ass
ess the role that eosinophils play in larval killing. Treated animals
showed no decrease in immunity when challenge infections consisted of
systemically migrating L3 administered 3 weeks after booster immunizat
ions. Eosinophil numbers in immunized mice decreased to control levels
when measured 3 weeks post-booster immunization, both in diffusion ch
ambers and in the peripheral blood, whereas they were elevated at 1 we
ek after booster immunizations. Direct contact between host cells and
L3 was, however, still required for larval killing in immunized hosts
3 weeks after booster immunizations. Elimination of eosinophils by tre
atment with mAb to IL-5 or granulocytes significantly reduced protecti
ve immunity, when L3 were implanted in diffusion chambers at 1 and 3 w
eeks post-booster. However, as systemically migrating L3 were still ki
lled in immunized, eosinophil-depleted animals, other cell types may p
lay a role in larval destruction. Two human eosinophil granule product
s were found to be toxic for host-adapted L3(+), but had no effect on
infective L3, indicating that host-adapted larvae are possible targets
for eosinophil-mediated destruction of third stage larvae. These find
ings suggest that inactivation of eosinophils by mAb treatment abolish
es protective immunity to L3 contained within diffusion chambers and t
hat small numbers of eosinophils are sufficient for immune-mediated ki
lling of S. stercoralis L3. (C) 1996 Academic Press, Inc.