The regulatory effects of monocytes on human natural killer cells activated by lipopolysaccharides

Lipopolysaccharides (LPS) rapidly enhance cytotoxicity of human natural killer (NK) cells against tumor targets. The regulatory effects of peripheral blood monocytes (MO) on this activation were measured. When lymphocytes were kept at a constant number in culture containing LPS from oral and enteric...

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Veröffentlicht in:Journal of periodontal research Jg. 26; H. 6; S. 486
1. Verfasser: Lindemann, R A
Format: Journal Article
Sprache:Englisch
Veröffentlicht: United States 01.11.1991
Schlagworte:
Aggregatibacter actinomycetemcomitans
Cytotoxicity, Immunologic - drug effects
Dinoprostone - antagonists & inhibitors
Dinoprostone - pharmacology
Escherichia coli
Humans
Indomethacin - pharmacology
Interleukin-1 - pharmacology
Killer Cells, Natural - immunology
Lipopolysaccharides
Lymphocyte Activation - drug effects
Monocytes - immunology
Tumor Necrosis Factor-alpha - pharmacology
ISSN:0022-3484
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Zusammenfassung:Lipopolysaccharides (LPS) rapidly enhance cytotoxicity of human natural killer (NK) cells against tumor targets. The regulatory effects of peripheral blood monocytes (MO) on this activation were measured. When lymphocytes were kept at a constant number in culture containing LPS from oral and enteric bacteria, increasing the percentage of MO caused a dose-dependent suppression of NK cytotoxicity. This suppression was reversed by adding the prostaglandin (PG) inhibitor indomethacin which indicates that PGE was released by MO stimulated by LPS. PGE is known to suppress NK activity by its effects on cAMP. MO separated from lymphocytes by transwell membranes also suppressed NK cells in the presence of LPS but this action was again reversed by indomethacin. This suggests that cell-to-cell contact is not necessary for MO to suppress NK cytotoxicity when stimulated by LPS. The role of interleukin-1 (IL-1) and tumor necrosis factor (TNF) in NK suppression was studied. Antibodies to IL-1 and TNF did not alter the suppression mediated by MO on NK activity. Adding IL-1 or TNF to cell cultures without MO or LPS had no effect on NK activity after 24 h. TNF, but not IL-1, enhanced NK activity in the presence of LPS in cultures without MO. When PGE was preincubated with only lymphocytes for 2 h, the activating effects of a secondary stimulation, interleukin-2 (IL-2), were inhibited. IL-1 had no effect on IL-2 activation when pre-incubated with PBL but TNF slightly enhanced IL-2-induced NK cytotoxicity.
Bibliographie:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0022-3484
DOI:10.1111/j.1600-0765.1991.tb01799.x