Interaction of liposomes with Kupffer cells in vitro

Dijkstra, J.W.; Galen, W.; Hulstaert, C.E.; Kalicharan, D.; Roerdink, Frits H.; Scherphof, Gl

doi:10.1016/0014-4827(84)90711-0

Cited by 101 publications

(48 citation statements)

References 29 publications

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“…The negatively charged liposomes used here have been shown to be endocytosed rapidly by Kupffer cells [171, and endothelial cells present in our hepatic cell preparation do not take up liposomes [15]. Since the main mechanism of interaction of liposomes with Kupffer cells in vitro is adsorptive endocytosis [18], we examined the effect of cholesterol and serum on adsorption of liposomes at 4°C. At this temperature liposomes are predominantly adsorbed onto the cell surface and not phagocytosed [18].…”

Section: Resultsmentioning

confidence: 99%

“…Since the main mechanism of interaction of liposomes with Kupffer cells in vitro is adsorptive endocytosis [18], we examined the effect of cholesterol and serum on adsorption of liposomes at 4°C. At this temperature liposomes are predominantly adsorbed onto the cell surface and not phagocytosed [18]. It was found (see table 1) that the presence of cholesterol in liposomes reduces adsorption and serum further hinders this process for all liposomes in hepatic and splenic cells except the adsorption of cholesterol-rich liposomes on splenic ceils which, in contrast, is enhanced.…”

Section: Resultsmentioning

confidence: 99%

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Tissue specific opsonins for phagocytic cells and their different affinity for cholesterol‐rich liposomes

1988

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In accordance with the finding of our in vivo experiments reported earlier [(1983) Biochim. Biophys. Acta 761,142-157; (1986) Biochim. Biophys. Acta 888, 184-190], the results of in vitro experiments show that Kupffer cells avidly take up cholesterol-poor but not cholesterol-rich liposomes, whereas splenic phagocytic cells take up preferentially cholesterolrich rather than cholesterol-poor liposomes in the presence of serum. Evidence presented here suggests that serum contains opsonins specific for hepatic and splenic phagocytic cells and these opsonins have different affinities for cholesterolrich and cholesterol-poor liposomes.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Tissue specific opsonins for phagocytic cells and their different affinity for cholesterol‐rich liposomes

1988

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“…Such a system in vitro provides the most direct approach to investigate the mechanism of liposome-Kupffer cell interaction and to answer questions arising from studies in vivo [2,61. From a previous study we concluded that the major mechanism by which liposomes, at 37"C, interact with Kupffer cells is a process of adsorptive endocytosis [4]. After internalization of the vesicles, radioactively labeled lipid and encapsulated protein were both effectively degraded by the cells.…”

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confidence: 91%

“…Fluorescence and electron microscopic observations indicated that the lysosomes are the intracellular degradation sites of the liposomal components and a study of the effects of lysosomotropic amines on uptake and degradation of liposomal constituents confirmed the involvement of the lysosomal system in the breakdown of internalized vesicles [55]. In comparison with the almost complete degradation of entrapped albumin, liposomal phospholipid was degraded to a much lower extent [5].…”

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confidence: 96%

Uptake and processing of liposomal phospholipids by Kupffer cells in vitro

Dijkstra

Galen

Regts

et al. 1985

European Journal of Biochemistry

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We investigated the intracellular metabolic fate of choline-labeled phosphatidylcholines and sphingomyelin taken up by rat Kupffer cells in maintenance culture during interaction with large unilamellar liposomes composed of cholesterol, labeled choline-phospholipid and phosphatidylserine (molar ration 5 : 4 : 1).With both labeled compounds only small proportions of water-soluble radioactivity were found to accumulate in the cells and in the culture medium, suggesting limited phospholipid degradation. However, after a lag period of 30 min progressively increasing proportions of cell-associated liposomal phospholipid were found to be converted to cellular phospholipid, nearly all of which was phosphatidylcholine. This conversion as well as the limited release of watersoluble label from the cells was inhibited by the lysosomotropic agents ammonium chloride and chloroquine.With [Me-'4C]choline-labeled lysophosphatidylcholine, label was found to become cell-associated far in excess of an encapsulated liposomal label, [3H]inulin. Without a lag period virtually all of this was rapidly converted to phosphatidylcholine, a process which was not inhibited by the lysosomotropic agents..It is concluded that Kupffer cells, after endocytosis of liposomes, degrade the liposomal phospholipids effectively but reutilize the choline moiety for de novo synthesis of cellular phosphatidylcholine.

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“…In at least one case the affinity of the MHC for reconstiOne of the better known observations in the cell tution into liposomes was so great that a liposome biology of liposomes is that liposomes are taken up reconstitution procedure was actually suggested as a avidly by macrophages both in vitro [40][41][42][43][44][45][46][47], and in method for purifying the MHC [30]. An interesting vivo .…”

Section: Ij-d Interactions Of Liposomes With Antigen Presentingmentioning

confidence: 99%