The mechanism of eosinophil accumulation in the cerebrospinal fluid of Angiostrongylus cantonensis infected hosts

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Results obtained are summatrized as follows : 1. Eosinophil accumulation in nonpermissive host (mice) : Cerebrospinal fluid (CSF) eosinophils collected from AF heterozygous (nu/+) mice infected with Angiostrongylus cantonensis (A.c) for 20 days or peritoneal eosinophils harvested from the peritoneal cavity of nu/+ mice infected with Mesocestoides corti (M.c) for 20 days were iv rtansferred into uninfected, normal nu/nu mice or into those infected with A.c for 17 days. Eosinophil accumulation in CSF occurred in only A.c-infected nu/nu mice transferred with eosinophils. A.c-infected nu/nu mice with CSF eosinophilia showed significantly low intracranial worm recovery. A combined injection of spleen cells from A.c-infected nu/+ mice along with CSF eosinophils caused the suppression of eosinophil accumulation in the CSF of A.c-infected nu/nu mice. Transfers of fluorochrome-labeled eosinophils from CSF or peritoneal cavity indicated that almost all eosinophils accumulated in the CSF of the recipient nu/nu mice were transferred-eosinophils themselves. These data suggest that the pre-existence of intracranial worms in the recipient mice is a prersquisite for CSF eosinophil accumulation and also that CSF eosinophilia is involved in the killing of intracranial worms. 2. Eosinophil accumulation in permissive host (rats) : Intraventricular injection of A.c-young adult worm (YA) antigen, A.c-egg antigen, or M.c antigen was performed in rats with peripheral eosinophilia due to (1)A.c infection for 40-43 days, (2) M.c infection for 20-23 days and (3) A.c-adult worm infection for 22-23 days following intrapulmonary transfers of YA.Monitoring of CSF eosinophilia in these rat groups indicated that CSF eosinophil accumulation occurred in A.c-infected rats following injection with A.c-egg or M.c antigen but not with YA antigen. These findings coincide with in vitro chemotactic activity of A.c-egg and M.c antigens against rat-eosinophils. It seems likely that the induction of eosinophi