RAT KUPFFER CELL ACTIVITY 917 irradiation for maximum protection indicates that it does not act in the circulating blood.As in animals in shock ( 10) , increased plasma acid phosphatase was consistently associated with early radiation death in the young chick. While a 2-fold or greater increase in PAPase activity was demonstrated in 1eth.ally irradiated chicks ( 1 2~1 5 0 0 R Y o gamma rays) only small increases were demonstrated in groups that received nearlethal exposures (700 R) or that were protected by SBTI administered before a lethal exposure. The increase in PAPase after a lethal irradiation is probably a secondary effect, reflecting release of excess hydrolases from damaged cells. An increase in plasma enzyme before 2 hours would be expected if such a change were a significant factor in initiating the vascular degeneration observed within a few hours after irradiation. Although contributions from circulating substances to this effect cannot be discounted entirely, available evidence supports the involvement of a direct effect. Observations on the circulation in small blood vessels in irradiated chick embryos indicate that degenerative changes occur in localized areas of the vascular wall ( 3 ) .Summary. Soybean trypsin inhibitor (SBTI) can act to reduce early radiation lethality (<24 hours) in the 3-day chick as well as in the 14-day chick embryo. Plasma acid phosphatase activity was increased more than 2-fold in lethally irradiated chicks, but only small increases were demonstrated in groups that received near-lethal exposures or that were protected by SBTI before a lethal exposure. ~~ 1. Christian, E.
The key role of the macrophage as the afferent component of the immune reflex arc is well documented (6-8, 10, 11, 19, 22, 31). Furthermore, Frei et al. (9) demonstrated that phagocytosis is an essential step in the development of the primary immune response while others have shown that the transplantation of macrophages into newborn mice ( 1 ) and rabbits (19) will promote the early development of immunocompetence. In view of these findings, it would be expected that the administration of chemotherapeutic agents which alter the normal phagocytic function of the reticuloendothelial system (RES) would induce a corresponding alteration in the immune response. Indeed, Wooles and Di Luzio (31) initially demonstrated that RES depression was associated with a decreased immune response while RES stimulation resulted in an increased antibody titer.Previous studies from this laboratory ( 2 5 ) have shown that a single injection of antilymphocytic serum (ALS) impairs phagocytic activity of the reticuloendothelial system (RES), as reflected by a depressed intravascular clearance rate of gelatinized RE test lipid emulsion. The ALS-induced depression in phagocytosis was associated with a selective decrease in Kupffer cell phagocytosis. In vitro studies which employed both serum and liver slices derived from either normal or ALS-treated animals also indicated the ability of ALS to induce phagocytic impairment, These in vitro studies (25) suggested that the depression of RES activity by ALS could be attributed to an exclusive defect in the cellular compartment of the RES since no Supported, in part, by the U. S. Army Medical Research and Development Command, the Atomic Energy Commission, and the Cancer Association of Greater New Orleans, Inc. alterationin circulating phagocyticpromoting activity was found in ALS-treated animals. Furthermore, a direct injurious effect of ALS on Kupffer cells was demonstrated, not only by ALS-induced impairment of Kupffer cell phagocytic activity, but also by the cytotoxic action of ALS on these macrophages (25). These studies suggested the distinct possibility that ALS-induced immunosuppression may be mediated by an alteration of RES function which results from the antimacrophage activity manifested by ALS (25) Antilymphocytic serum has been shown to be an effective immunosuppressant of both cellular (13, 20, 29) and humoral immune responses (14, 20, 29). Indeed, ALS has been employed extensively in renal transplan tation (23, 28, 31) despite the fact that the mode of action of ALS-induced immunosuppression is as yet unclarified (13, 15, 16, 20, 26). In view of our previous observations of the detrimental effect of ALS on Kupffer cell viability and function (25), studies were undertaken to evaluate the influence of hepatic as well as peritoneal and splenic macrophage transplantation on ALS-induced immunosuppression. Studies were also extended to determine the ability of splenic and thymic lymphocytes to restore the humoral antibody response in ALS-immunosuppressed animals.Materials and Method...
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