Abstract
Chemical inhibitors of immediate hypersensitivity were used to treat rats passively immunized against Taenia taeniaeformis with serum containing 7Sγ2a and reaginic antibodies. There was no significant reduction in protection against oral challenge with eggs in these animals, indicating that reagin-mediated hypersensitivity reactions were not an essential component of the protective mechanism. However, systemic reagin sensitization was shown to result in an acceleration of the rate at which challenge organisms were destroyed in immune rats. By 12 h after infection most of the parasites had been killed in the livers of rats which had been both passively immunized and reagin-sensitized, whereas a large proportion survived in rats passively immunized, but not reagin-sensitized. This effect of reagin appeared to be limited to the early stages of resistance since parallel groups left for 21 days after challenge were shown to have been equally well protected.
In an effort to determine if vasoactive amines liberated by reagin-mediated reactions could act directly on invading parasites, early larval stages of T. taeniaeformis were exposed to histamine or serotonin (5HT) in vitro or in vivo. Consistent results were not obtained, but significant inhibition (P<0.05) of viability of parasites exposed to histamine occurred on two occasions. Significant (P<0.01) inhibition of infectivity of T. taeniaeformis also resulted when peritoneal anaphylactic diffusate was introduced into isolated gut loops containing hatched embryos of the parasite. The results are discussed in terms of the possible means whereby reagins may participate in protective immunity to infectious organisms.
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