Mice were exposed to different intensities of infection with Schistosoma mansoni (10, 50, or 200 cercariae) and the kinetics of peripheral and bone marrow eosinophilia was followed for as long as 20 wk. When the schistosomula (immature worms) were migrating from the lungs to the liver there was a mild, transient eosinophilia, but soon after the onset of egg laying by the schistosomes, a major and prolonged increase in eosinophils occurred. This was terminated in the heavier infections by the death of the animals, but showed a spontaneous decline beginning at 18 wk in the lightly infected mice. The effect of S. mansoni eggs on eosinophilia in the blood, bone marrow, and granulomatous lesions was then examined by injecting schistosome eggs into mice intraperitoneally, subcutaneously, and intravenously. While the host response was dependent on the route by which eggs were administered, primary peripheral and bone marrow responses were seen on intravenous injection, and secondary responses occurred on intravenous and subcutaneous injection. In unsensitized and egg-sensitized mice, eosinophils were first seen around eggs injected into the pulmonary microvasculature at 96 and 24 h respectively. When the granulomas were maximal in size eosinophils made up at least 50% of the lesions. Administration of antieosinophil serum profoundly suppressed eosinophils in the peripheral blood, eliminated mature eosinophils and markedly increased eosinophil precursors in the bone marrow, and ablated eosinophils from the tissue lesions, considerably reducing their area.

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