MODULATION OF PHAGOCYTOSIS BY ANISOOSMOLARITY AND BETAINE IN RAT-LIVER MACROPHAGES (KUPFFER CELLS) AND RAW-264.7 MOUSE MACROPHAGES

Hypoosmotic exposure (205 mosmol/l) of rat liver macrophages (Kupffer cells) for 12 h stimulated phagocytosis of latex particles by about 20 %, whereas hyperosmotic exposure (405 mosmol/l) resulted in 30-40% inh ibition, Inhibition of phagocytosis by hyperosmolarity was fully preve nted in the presence of betaine, which acts as an osmolyte in liver ma crophages, When hyperosmotically exposed Kupffer cells were preloaded with betaine, induction of phagocytosis by addition of latex particles led to the stimulation of betaine efflux from the cells, Stimulation of phagocytosis also inhibited the hyperosmolarity-induced cumulative uptake of betaine into Kupffer cells, but did not prevent the hyperosm olarity-induced increase in BGT1-mRNA levels, Whereas these findings s uggest an involvement of cell volume and betaine in the regulation of phagocytosis in Kupffer cells, betaine transport was not affected upon induction of phagocytosis in RAW 264.7 mouse macrophages, The finding s are compatible with a role of betaine in maintaining cell volume hom eostasis during phagocytosis in Kupffer cells, but not in RAW 264.7 mo use macrophages, This may be relevant for the maintenance of liver hem odynamics, since volume changes of liver macrophages following ingesti on of phagocytozable material might otherwise impair sinusoidal perfus ion.