Inhibitory effect of cholesterol on the uptake of liposomes by liver and spleen
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Mononuclear phagocyte system
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The interpretation of a number of diseases associated with splenomegaly presents significant difficulties; this is due to the fact that the role of the spleen in them is not well understood. The leading role of the spleen in the phenomena of erythrophagocytosis has been most firmly established. The spleen is also one of the most powerful organs of the reticuloendothelial system.
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Using a modified aerosol generator, white mice and calves were exposed to aerosols of viable Staphylococcus aureus and Pasteurella haemolytica and the clearance of the inhaled organisms by the lungs of the experimental animals was measured. Fifty-seven percent of inhaled S. aureus were cleared in two hours by the mouse lungs, 79% were cleared in four hours and 93% were cleared in eight hours. Fifty-six percent of inhaled P. haemolytica were cleared in two hours by the mouse lungs, 76% were cleared in four hours and 93% were cleared in eight hours. Seventy percent of inhaled S. aureus were cleared in two hours by the calf lungs, 90% were cleared in four hours and 95% were cleared in eight hours. Seventy-five percent of inhaled P.haemolytica were cleared in two hours by the calf lungs, 90% were cleared in four hours and 92% were cleared in eight hours.
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Liposomes have a pronounced tendency to localize in the reticuloendothelial (RE) system, a major host defense system. We have examined, in mice, the effect of chronic i.v. administration of low to moderate liposome doses on drug metabolism, phagocytic index and spleen and liver size. Little effect on the rate of pentobarbital metabolism was noted, except when mice received 80 mg/kg of sphingomyelin-containing liposomes in a series of 10 injections over 3.5 weeks. Impairment of RE phagocytic function was found to be related to liposome size and composition, size and frequency of liposome dose and the presence of lipid peroxides. The effects on tissue distribution of liposome-entrapped [14C]sucrose was also determined in mice receiving chronic liposome injections. In RE blockaded mice there was a consistent trend in favor of decreased liver uptake and increased spleen uptake. No significant uptake of liposome contents was seen in non-RE tissues even in mice with severe RE blockade, indicating that the induction of RE blockade by predosing with empty liposomes may not be a successful strategy for increasing liposome uptake to non-RE tissues. Liver to spleen ratios of [14C]sucrose appeared to be a sensitive method for quantitating RE blockade. Sphingomyelin-containing liposomes produced the greatest RE blockade, distearoylphosphatidylcholine-cholesterol liposomes were intermediate and egg phosphatidylcholine-cholesterol liposomes produced the least impairment in RE function. Liposomes which contained 1% vitamin E as an antioxidant had slightly less effect on RE function than liposomes not containing vitamin E.(ABSTRACT TRUNCATED AT 250 WORDS)
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Experiments were undertaken, with rats, to determine whether the spleen plays a role in choline chloride-induced reticuloendothelial system (RES) phagocytic stimulation and protection against circulatory shock. Choline pretreatment of normal, intact, but not splenectomized rats, resulted in heightened RES phagocytic stimulation and protection against acute hemorrhagic shock. Choline pretreatment significantly increased spleen size in normal intact rats. Wet liver or lung weights were not significantly affected by choline pretreatment of either normal or splenectomized rats. Untreated, splenectomized animals did not demonstrate any significant alterations in either RES phagocytic activity or RE organ wet weights when compared to normal, intact controls or to sham-operated animals. Although the results of these experiments make it clear that the presence of a functioning spleen is necessary for choline-induced RES stimulation and shock protection, it is not clear as to just how these actions are brought about. Further exploration is warranted in view of the clinical implications of these findings.
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The interaction of liposomes derived from total lipids of mouse spleen and liver with mouse spleen cells was studied. It was shown that the binding of these liposomes is much higher than the binding of liposomes obtained from a model lipid mixture--phosphatidylcholine--phosphatidylethanolamine--cholesterol (2:1:1). Adherent and nonadherent spleen cells were found to have affinity for liposomes derived from total lipids of spleen or liver. Removal of gangliosides and protein contaminants from the liposomes derived from total spleen lipids caused an increased binding of liposomes to spleen cells. Multilamellar liposomes bound more effectively to ultrasonicated vesicles having a homologous lipid composition than the liposomes with a different lipid composition. The increased affinity of liposomes derived from total lipids of spleen or liver for spleen cells may account for the identical fluidity of the lipid bilayer of liposomes and plasma membranes of spleen cells.
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The effects of encapsulation of carboquone (CQ) in the liposomes were investigated on the plasma clearance and tissue distribution of CQ in rabbit and rat. CQ-Liposome, the liposomes in which CQ was encapsulated, was prepared by the method described in a previous report. By intravenous administration at the same dose. CQ-liposome showed approximately three times higher plasma concentration than free CQ in rabbit and rat. However, prolonged release from liposomes or stabilization of CQ in plasma was not observed by encapsulation. The distribution to lung and reticuloendothelial-rich organs such as liver and spleen was enhanced, but on the contrary the distribution to the peripheral tissues such as muscle and skin was decreased. In rats pretreated with drug free liposomes, high plasma CQ concentration was obtained after intravenous administration of CQ-liposome. From these results, it is considered that the large parts of CQ-liposome is distributed into reticuloendothelial system (RES) and RES is saturable with liposomes. And it is also presumed that the high plasma concentration obtained after intravenous administration of CQ-liposome, would be caused by altering the tissue distribution of CQ by encapsulation.
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