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Blood, Vol. 93 No. 11 (June 1), 1999:
pp. 4011-4018
Lipopolysaccharide Regulates Macrophage Fluid Phase Pinocytosis Via
CD14-Dependent and CD14-Independent Pathways
Maikel P. Peppelenbosch,
Marjory DeSmedt,
Tessa ten Hove,
Sander
J.H. van Deventer, and
Johan Grooten
From Laboratory for Experimental Internal Medicine, G2-130 Academic
Medical Centre, Amsterdam, The Netherlands; and Laboratory for
Molecular Biology, Flemish Institute for Biotechnology, G, Belgium.
Lipopolysaccharide (LPS) is a mediator of inflammation and septic
shock during bacterial infection. Although monocytes and macrophages
are highly responsive to LPS, the biological effects of LPS in these
cell types are only partially understood. We decided, therefore, to
investigate the influence of LPS on macrophage pinocytosis and Fc
receptor-mediated endocytosis, two prominent and related macrophage
effector functions. We observed that LPS did not greatly influence
endocytosis in either macrophages or monocytes, but did exert a dual
action on pinocytosis: at lower concentrations (0.1 to 100 ng/mL), LPS
caused a decrease in pinocytosis in both macrophages and monocytes,
whereas at higher LPS concentrations, enhanced pinocytosis in
macrophages was observed. Detoxified LPS was two orders of magnitude
less potent in producing these effects. After inhibition of the LPS
receptor CD14, the LPS-induced decrease in pinocytosis was absent, and
stimulation of pinocytosis at lower LPS concentrations was unmasked. We
conclude that LPS can influence pinocytosis via CD14-dependent and
CD14-independent signaling pathways. Furthermore, as
addition of LPS to macrophages effected pinocytosis but not Fc
receptor-mediated endocytosis, these two processes are independently
regulated in macrophages.
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