ELEVATED INNATE PERIPHERAL-BLOOD EOSINOPHILIA FAILS TO AUGMENT IRRADIATED CERCARIAL VACCINE-INDUCED RESISTANCE TO SCHISTOSOMA-MANSONI IN IL-5 TRANSGENIC MICE

Numerous factors contribute to host resistance to infection with Schis tosoma mansoni. Although several studies have investigated the eosinop hil as an effector cell of protective responses, its true role remains unclear. In vitro, human, but not mouse, eosinophils can kill schisto somula. Studies on schistosome infection susceptibility in naive or va ccinated eosinophil-deficient mice have yielded conflicting results. U sing the gamma-irradiated cercariae (irr-cerc) model, we vaccinated in terleukin (IL)-5 transgenic mice in parallel with background-matched c ontrols (C3H/HeN) to examine whether innate eosinophilia contributes t o increased protection from a challenge infection. In our laboratory, mean peripheral blood eosinophil (PBE) levels in IL-5 transgenic mice were 21,000 mm(3), whereas in naive C3H/HeN mice this value was 240 mm (3). In 3 separate experiments, both groups of vaccinated mice showed significant resistance to challenge infection. However, there was no s ignificant difference in the percent worm reduction between transgenic IL-5 C3H mice (mean % protection = 44.3; range = 42-45%) and the cont rol C3H/HeN mice (mean % protection = 51.7; range = 41-64%). Our findi ngs indicate that high levels of innate PEE due to constitutive produc tion of IL-5 do not augment irr-cerc-stimulated immunity.