Bacterial Lipopeptides Induce Nitric Oxide Synthase and Promote Apoptosis through Nitric Oxide-independent Pathways in Rat Macrophages (∗)

Stimulation of resident peritoneal macrophages with S-[2,3-bis(pamitoyloxy)-(2R,2S)-propyl]-N-palmytoyl-(R)-CysSerLys4 or S-[2,3-bis(pamitoyloxy)-(2R,2S)-propyl]-N-palmytoyl-(R)-CysAlaLys4, two synthetic bacterial lipopeptides, promoted the expression of the inducible form of nitric oxide synthase,...

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Veröffentlicht in:The Journal of biological chemistry 1995-03, Vol.270 (11), p.6017-6021
Hauptverfasser: Terenzi, Fulvia, Díaz-Guerra, María J.M., Casado, Marta, Hortelano, Sonsoles, Leoni, Silvia, Boscá, Lisardo
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container_end_page 6021
container_issue 11
container_start_page 6017
container_title The Journal of biological chemistry
container_volume 270
creator Terenzi, Fulvia
Díaz-Guerra, María J.M.
Casado, Marta
Hortelano, Sonsoles
Leoni, Silvia
Boscá, Lisardo
description Stimulation of resident peritoneal macrophages with S-[2,3-bis(pamitoyloxy)-(2R,2S)-propyl]-N-palmytoyl-(R)-CysSerLys4 or S-[2,3-bis(pamitoyloxy)-(2R,2S)-propyl]-N-palmytoyl-(R)-CysAlaLys4, two synthetic bacterial lipopeptides, promoted the expression of the inducible form of nitric oxide synthase, exhibiting a temporal pattern of nitric oxide release that was delayed with respect to the induction elicited by bacterial lipopolysaccharide. Treatment of macrophages with genistein blocked the nitric oxide synthesis triggered by the lipopeptides or lipopolysaccharide. Simultaneous incubation with lipopolysaccharide and lipopeptide resulted in an antagonistic effect on nitric oxide synthase mRNA levels and on nitrite plus nitrate release to the medium. Triggering with bacterial lipopeptides induced macrophage programmed cell death. In macrophages activated with lipopeptide, apoptosis was observed even in the absence of nitric oxide synthesis, therefore indicating the existence of alternative pathways in the control of programmed cell death in these cells.
doi_str_mv 10.1074/jbc.270.11.6017
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Treatment of macrophages with genistein blocked the nitric oxide synthesis triggered by the lipopeptides or lipopolysaccharide. Simultaneous incubation with lipopolysaccharide and lipopeptide resulted in an antagonistic effect on nitric oxide synthase mRNA levels and on nitrite plus nitrate release to the medium. Triggering with bacterial lipopeptides induced macrophage programmed cell death. 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Treatment of macrophages with genistein blocked the nitric oxide synthesis triggered by the lipopeptides or lipopolysaccharide. Simultaneous incubation with lipopolysaccharide and lipopeptide resulted in an antagonistic effect on nitric oxide synthase mRNA levels and on nitrite plus nitrate release to the medium. Triggering with bacterial lipopeptides induced macrophage programmed cell death. 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subjects Amino Acid Oxidoreductases - biosynthesis
Amino Acid Sequence
Animals
Apoptosis - drug effects
Cells, Cultured
Cytokines - pharmacology
Dose-Response Relationship, Drug
Enzyme Induction
Genistein
Growth Inhibitors - pharmacology
Hydrogen Peroxide - metabolism
Interferon-alpha - pharmacology
Interferon-gamma - pharmacology
Isoflavones - pharmacology
Lipopolysaccharides - pharmacology
Lipoproteins - pharmacology
Macrophages, Peritoneal - cytology
Macrophages, Peritoneal - drug effects
Macrophages, Peritoneal - metabolism
Male
Molecular Sequence Data
Nitric Oxide - physiology
Nitric Oxide Synthase
Phorbol 12,13-Dibutyrate - pharmacology
Rats
Structure-Activity Relationship
Tumor Necrosis Factor-alpha - pharmacology
title Bacterial Lipopeptides Induce Nitric Oxide Synthase and Promote Apoptosis through Nitric Oxide-independent Pathways in Rat Macrophages (∗)
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