Reaginic antibody response in rabbits infected with Taenia pisiformis.
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Biomedical subjects
Publications and source records attributed to R W Leid.
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Weanling rats born of mothers infected with Taenia taeniaeformis were found to be passively protected against homologous challenge. Cross-fostering of normal suckling rats onto immune mothers established that passive transfer occurred via the colostrum and milk. Immunoglobulin fractions containing gammaA from immune colostrum were fed to 12-14-day-old rats for 4 days via stomach tube. Significant passive protection against challenge with T. taeniaeformis was achieved with gammaA from one of three colostrum pools. The effect of colostral gammaA preparations on the infectivity of freshly hatched oncopheres of T. taeniaeformis was measured by the intra-intestinal inoculation of immunoglobulin solutions into isolated gut loops containing hatched eggs of the parasite. gammaA from one of three pools of immune colostrum caused a significant reduction in the number of parasites which reached the liver. This appears to be the first time that protective activity against a helminth infection has been achieved with gammaA. A fraction of immune colostrum containing both 7Sgamma1 and 7Sgamma2 immunoglobulins was found to confer passive protection when inoculated parenterally. In view of the prolonged period of absorption (ca 18 days) of 7S immunoglobulins from the gut by the suckling rat, it seems likely that these antibodies are primarily responsible for the natural passive transfer of protection from mother to young.
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Bovine alveolar macrophages (BAM) prelabeled with 3H-arachidonic acid (AA) were exposed in vitro to different doses of DQ-12, Minusil-5, and Sigma silicas, or carbonyl iron beads. Arachidonic acid metabolites released into the culture medium by BAM were identified and quantitated using high performance liquid chromatography (HPLC). Cytotoxicity was assessed by the release of lactate dehydrogenase (LDH). At doses of 0.1 or 0.25 mg of DQ-12 silica and of 0.25 or 0.5 mg of Minusil-5 and Sigma silica, the release of cyclooxygenase metabolites (TXB2, PGE2, PGF2, and HHT) comprised greater than 95% of the total released AA metabolites. Silica doses above 0.5 mg led to 5-lipoxygenase metabolite release (LTB4, its two nonenzymatic isomers, and 5-HETE). This shift to 5-lipoxygenase metabolite release paralleled increased cellular cytotoxicity and was observed for each of the silicas. In contrast to silica stimulation, carbonyl iron beads elicited only small quantities of cyclooxygenase metabolites, no 5-lipoxygenase metabolites, and showed little cytotoxicity toward BAM. The relative potency of each particulate for stimulating the release of AA metabolites and LDH was calculated with DQ-12 greater than Minusil-5 greater than Sigma much greater than carbonyl iron beads. Our results indicate that the cytotoxic and presumed fibrogenic potential of a silica may be correlated with the potency to stimulate the release of 5-lipoxygenase metabolites from AM.