Bacterial lipopolysaccharide suppresses the expression of lipoprotein lipase in murine macrophages: a process independent of tumor necrosis factor or interleukin 1

Abstract

Lipopolysaccharide (LPS) modulates macrophage functions and induces the synthesis and secretion of tumor necrosis factor (TNF) and interleukin 1 (IL-1) in these cells. The latter two factors but not LPS suppress lipoprotein lipase (LPL) synthesis and secretion in adipocytes. Since the regulation of LPL secretion in macrophages is rather poorly understood, we investigated the effect of the macrophage activator LPS on LPL secretion by macrophages. LPS suppressed in a dose- and time-dependent manner the heparin-induced secretion of LPL from the macrophage-like tumor cell line J774.1 and from bone marrow derived mononuclear phagocytes (BMM). Suppression of LPL secretion from J774.1 and that from BMM reached about 66 and 50%, respectively, within 8 h of exposure to 500 ng/ml LPS. LPS did not inhibit the enzymic activity of LPL when added directly to the cell free enzyme assay system. Human recombinant TNF (1000 U/ml) and murine recombinant IL-1 (100 U/ml) did not affect LPL secretion or cell proliferation in the J774.1 cell line over a period of 72 and 24 h, respectively. Thus LPS regulates macrophage secretion of LPL in a mechanism independent of the induction of autocrine production of TNF and IL-1, and possesses a disparate pattern of regulation to that expressed by adipose tissue cells.