The role of the spleen in controlling the number of microfilariae (Dirofilaria immitis, D. repens, Litomosoides carinii and Dipetalonema witei) in the blood.
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Histologic changes occurring in the rabbit spleen during the primary response to intravenous injection of bovine gamma globulin alone and in combination with bacterial endotoxin have been described. The predominant morphologic changes associated with antibody formation in animals that received antigen alone were confined to the follicular areas of the spleen. Only minimal changes were seen in the red pulp. No new cellular types appeared following endotoxin stimulus. Rather, a profound augmentation of events observed following a single injection of bovine gamma globulin alone appears to account for the higher levels of antibody incited by this adjuvant. The cell type important in antibody formation under these conditions appeared to be a modified reticular cell. Plasma cells were not part of the cellular reaction. A hypothesis describing the primary antibody response is presented.
The uptake of intravenously injected coconut oil emulsion by the liver and spleen was investigated by gas-liquid chromatography in normal, triton-injected, and hypercholesterolemic rabbits. The lauric and myristic acids from this emulsion, almost absent in the tissues of normal animals, were used as marked acids. In normal rabbits only the liver took up a quantitatively important fraction of the injected fat. The uptake by the spleen appears to be due to a different mechanism than that of the liver. In rabbits given triton the liver was incapable of taking up large quantities of fat, while the uptake in the spleen was undisturbed. 12 hours after injection the plasma, liver, and spleen of normal animals contained only 14 per cent of the dose. With animals given triton 71 per cent of the injected dose was recovered, most of it in the plasma. Hypercholesterolemic rabbits cleared an injected fat emulsion and took fat into the liver at the same rate as the controls. When triton is injected 6 hours after the administration of the emulsion, the fat taken up in the liver reappears in the plasma.
Rats thymectomized at birth gained weight and otherwise developed normally, but were found to be very susceptible to intercurrent infections. Both Arthus reactivity and delayed hypersensitivity to BSA were markedly impaired in rats thymectomized during the first week of life and significantly impaired in rats thymectomized as late as 3 weeks after birth. The inhibition of Arthus reactivity in thymectomized rats was well correlated with their failure to develop significant titers of precipitating or hemagglutinating antibody. However, natural heteroagglutinin titers were not altered in these animals, and no abnormality of serum proteins, including gamma-globulin could be detected by paper electrophoresis. The loss of immunologic activity could not be corrected by injecting homogenates of spleen or thymus before and during the sensitization period. Splenectomy at birth did not influence Arthus or delayed reactivity.
Antibody formation in vitro by red and white pulp of the spleen and by bone marrow tissue was studied at various days after an intravenous booster injection of soluble antigens such as ovalbumin and bovine gamma globulin (BGG). When the booster injection of antigen was given early (10 days) after an intravenous primary injection, high antibody formation could be demonstrated in the spleen primarily 2 to 3 days after the injection, but much less afterwards. When the booster injection was given later (1 month) after the primary, the antibody production by the spleen lasted longer and higher serum titers were obtained. The bone marrow formed antibody in both cases but, particularly with the short interval between injections, its response was delayed as compared to the spleen. It was also shown that during antibody formation the production of gamma globulin in vitro was enhanced. Histologically the antibody production was always correlated to immature plasma cell proliferation, located at the border of red and white pulp and in the red pulp of the spleen. When endotoxin had been injected at the time of a primary BGG injection, and a second antigen injection was given 5 to 10 days later, a booster response could be elicited which was sometimes limited to the white pulp on day 1, and on day 2 was divided between "red" and "white" pulp. The response induced at day 10, at the peak of secondary nodule proliferation, lasted very long and was accompanied by an enormous plasma cellular proliferation in and around the periarteriolar lymphoid areas of the spleen. The possible importance of the secondary nodules of the white pulp in the preparation for a secondary response is discussed.
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