Characterization of patocytosis: endocytosis into macrophage surface-connected compartments

Previously, we described a unique macrophage endocytosis pathway in which a ggregated low density lipoproteins and microcrystalline cholesterol induce and enter a labyrinth of membrane-bound compartments that remain connected to the cell surface. We now show that certain types of non-lipid particles such as polystyrene microspheres and colloidal gold also induce and enter m acrophage surface-connected compartments (SCC), a process we call patocytos is, A common property among particles that stimulate patocytosis is their h ydrophobic nature. Both aggregated LDL and microcrystalline cholesterol tha t we showed previously to stimulate patocytosis are hydrophobic, We now sho w that hydrophobic polystyrene microspheres and gold particles but not thei r hydrophilic counterparts triggered patocytosis. Uptake by patocytosis was limited to hydrophobic polystyrene microsphere particles less than 0.5 mu m in diameter. Hydrophobic polystyrene microspheres greater than this size entered macrophages by phagocytosis, Actin-independent capping of hydrophob ic polystyrene microspheres on the plasma membrane preceded actin-dependent uptake of the microspheres into SCC. Sequential rounds of microsphere upta ke into SCC over two successive days could occur. There was some mixing of initial and subsequently accumulated microspheres in SCC, SCC formed from p lasma membrane invaginations that connected with spaces created by unfoldin g of stacks of internal microvilli. Microsphere transport from plasma membr ane invaginations into these spaces was inhibited by primaquine, patocytosi s is a unique endocytic process in macrophages triggered by small hydrophob ic particles that provides a mechanism to sequester large amounts of these materials within a labyrinth of SCC.