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Phagocyte function in familial hypercholesterolaemia: peripheral blood monocytes exposed to lipopolysaccharide show increased tumour necrosis factor production. 1990

M Leirisalo-Repo, and M Jäättelä, and H Gylling, and T A Miettinen, and H Repo
Department of Bacteriology and Immunology, University of Helsinki, Finland.

We studied functions of polymorphonuclear leucocytes (PMN) and monocytes from peripheral blood of subjects with familial hypercholesterolaemia (FH). FH monocytes exposed to Escherichia coli lipopolysaccharide (LPS) in 10% human AB serum generated tumour necrosis factor (TNF) significantly more than did control monocytes. After lowering of serum low-density lipoprotein (LDL) levels by drug treatment, FH monocytes exposed to LPS in the absence of exogenous lipoproteins generated significantly more TNF than did control monocytes. These findings suggest that increased TNF production is not affected by hypolipidaemic treatment and may not derive from differences between uptake of exogenous LDL by FH monocytes and control cells. Chemotaxis, chemokinesis, and random migration of both FH PMN and FH monocytes were normal, as determined by agarose assay and membrane filter assay. FH PMN showed increased luminol-enhanced chemiluminescence in response to 2.5 x 10(-8) M, but not to 2.5 x 10(-6) M, N-formyl-methionyl-leucyl-phenylalanine, and not to serum-treated zymosan or to phorbol myristate acetate. Luminol- and lucigenin-enhanced chemiluminescence responses of FH monocytes were normal. In summary, the major aberration found in the present study was that FH monocytes stimulated with LPS show enhanced production of TNF. The possibility that exaggerated TNF production contributes to an early development of atherosclerotic lesions in FH subjects warrants further studies.

UI MeSH Term Description Entries
D008070 Lipopolysaccharides Lipid-containing polysaccharides which are endotoxins and important group-specific antigens. They are often derived from the cell wall of gram-negative bacteria and induce immunoglobulin secretion. The lipopolysaccharide molecule consists of three parts: LIPID A, core polysaccharide, and O-specific chains (O ANTIGENS). When derived from Escherichia coli, lipopolysaccharides serve as polyclonal B-cell mitogens commonly used in laboratory immunology. (From Dorland, 28th ed) Lipopolysaccharide,Lipoglycans
D008297 Male Males
D008875 Middle Aged An adult aged 45 - 64 years. Middle Age
D009000 Monocytes Large, phagocytic mononuclear leukocytes produced in the vertebrate BONE MARROW and released into the BLOOD; contain a large, oval or somewhat indented nucleus surrounded by voluminous cytoplasm and numerous organelles. Monocyte
D009504 Neutrophils Granular leukocytes having a nucleus with three to five lobes connected by slender threads of chromatin, and cytoplasm containing fine inconspicuous granules and stainable by neutral dyes. LE Cells,Leukocytes, Polymorphonuclear,Polymorphonuclear Leukocytes,Polymorphonuclear Neutrophils,Neutrophil Band Cells,Band Cell, Neutrophil,Cell, LE,LE Cell,Leukocyte, Polymorphonuclear,Neutrophil,Neutrophil Band Cell,Neutrophil, Polymorphonuclear,Polymorphonuclear Leukocyte,Polymorphonuclear Neutrophil
D010586 Phagocytes Cells that can carry out the process of PHAGOCYTOSIS. Phagocyte,Phagocytic Cell,Phagocytic Cells,Cell, Phagocytic,Cells, Phagocytic
D002465 Cell Movement The movement of cells from one location to another. Distinguish from CYTOKINESIS which is the process of dividing the CYTOPLASM of a cell. Cell Migration,Locomotion, Cell,Migration, Cell,Motility, Cell,Movement, Cell,Cell Locomotion,Cell Motility,Cell Movements,Movements, Cell
D005260 Female Females
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D006938 Hyperlipoproteinemia Type II A group of familial disorders characterized by elevated circulating cholesterol contained in either LOW-DENSITY LIPOPROTEINS alone or also in VERY-LOW-DENSITY LIPOPROTEINS (pre-beta lipoproteins). Hyperbetalipoproteinemia,Hypercholesterolemia, Essential,Hypercholesterolemia, Familial,Apolipoprotein B-100, Familial Defective,Apolipoprotein B-100, Familial Ligand-Defective,Familial Combined Hyperlipoproteinemia,Hyper-Low Density Lipoproteinemia,Hyper-Low-Density-Lipoproteinemia,Hyper-beta-Lipoproteinemia,Hypercholesterolemia, Autosomal Dominant,Hypercholesterolemia, Autosomal Dominant, Type B,Hypercholesterolemic Xanthomatosis, Familial,Hyperlipoproteinemia Type 2,Hyperlipoproteinemia Type IIa,Hyperlipoproteinemia Type IIb,Hyperlipoproteinemia, Type II,Hyperlipoproteinemia, Type IIa,LDL Receptor Disorder,Apolipoprotein B 100, Familial Defective,Apolipoprotein B 100, Familial Ligand Defective,Autosomal Dominant Hypercholesterolemia,Autosomal Dominant Hypercholesterolemias,Combined Hyperlipoproteinemia, Familial,Combined Hyperlipoproteinemias, Familial,Density Lipoproteinemia, Hyper-Low,Density Lipoproteinemias, Hyper-Low,Disorder, LDL Receptor,Disorders, LDL Receptor,Dominant Hypercholesterolemia, Autosomal,Dominant Hypercholesterolemias, Autosomal,Essential Hypercholesterolemia,Essential Hypercholesterolemias,Familial Combined Hyperlipoproteinemias,Familial Hypercholesterolemia,Familial Hypercholesterolemias,Familial Hypercholesterolemic Xanthomatoses,Familial Hypercholesterolemic Xanthomatosis,Hyper Low Density Lipoproteinemia,Hyper beta Lipoproteinemia,Hyper-Low Density Lipoproteinemias,Hyper-Low-Density-Lipoproteinemias,Hyper-beta-Lipoproteinemias,Hyperbetalipoproteinemias,Hypercholesterolemias, Autosomal Dominant,Hypercholesterolemias, Essential,Hypercholesterolemias, Familial,Hypercholesterolemic Xanthomatoses, Familial,Hyperlipoproteinemia Type 2s,Hyperlipoproteinemia Type IIas,Hyperlipoproteinemia Type IIbs,Hyperlipoproteinemia Type IIs,Hyperlipoproteinemia, Familial Combined,Hyperlipoproteinemias, Familial Combined,Hyperlipoproteinemias, Type II,Hyperlipoproteinemias, Type IIa,LDL Receptor Disorders,Lipoproteinemia, Hyper-Low Density,Lipoproteinemias, Hyper-Low Density,Receptor Disorder, LDL,Receptor Disorders, LDL,Type 2, Hyperlipoproteinemia,Type II Hyperlipoproteinemia,Type II Hyperlipoproteinemias,Type IIa Hyperlipoproteinemia,Type IIa Hyperlipoproteinemias,Xanthomatoses, Familial Hypercholesterolemic,Xanthomatosis, Familial Hypercholesterolemic

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