Attenuated suppression of the oxidative burst by cells dying in the presence of oxidized low density lipoprotein[S]

Macrophages ingesting apoptotic cells attenuate inflammatory responses, such as reactive oxygen species (ROS) generation. In atherosclerosis, ongoing inflammation and accumulation of apoptotic/necrotic material are observed, suggesting defects of phagocytes in recognizing or responding to dying cell...

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Main Authors: Dmitry Namgaladze, Carla Jennewein, Stefan Preiss, Andreas von Knethen, Bernhard Brüne
Format: Article
Language:English
Published: Elsevier 2009-11-01
Series:Journal of Lipid Research
Subjects:
Online Access:http://www.sciencedirect.com/science/article/pii/S0022227520306830
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author Dmitry Namgaladze
Carla Jennewein
Stefan Preiss
Andreas von Knethen
Bernhard Brüne
author_facet Dmitry Namgaladze
Carla Jennewein
Stefan Preiss
Andreas von Knethen
Bernhard Brüne
author_sort Dmitry Namgaladze
collection DOAJ
description Macrophages ingesting apoptotic cells attenuate inflammatory responses, such as reactive oxygen species (ROS) generation. In atherosclerosis, ongoing inflammation and accumulation of apoptotic/necrotic material are observed, suggesting defects of phagocytes in recognizing or responding to dying cells. Modified lipoproteins such as oxidized LDL (oxLDL) are known to promote inflammation and to interfere with apoptotic cell clearance. Here, we studied the impact of cells exposed to oxLDL on their ability to interfere with the oxidative burst in phagocytes. In contrast to apoptotic cells, cells dying in response to or in the presence of oxLDL failed to suppress ROS generation despite efficiently being taken up by phagocytes. In addition, apoptotic cells, but not oxLDL-treated cells, inhibited phosphorylation of extracellular signal-regulated kinase, which is important for NADPH oxidase activation. oxLDL treatment did not interfere with activation of the antiinflammatory transcriptional regulator peroxisome proliferator-activated receptor γ by apoptotic cells. Moreover, cells exposed to oxLDL failed to suppress lipopolysaccharide- induced proinflammatory cytokine expression, whereas apoptotic cells attenuated these phagocyte responses. Thus, the presence of oxLDL during cell death impaired the ability of apoptotic cells to act antiinflammatory with regard to oxidative burst inhibition and cytokine expression in phagocytes.
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spelling doaj.art-7a96e0c22cdf454a84429a0270de211c2022-12-21T18:32:59ZengElsevierJournal of Lipid Research0022-22752009-11-01501121732181Attenuated suppression of the oxidative burst by cells dying in the presence of oxidized low density lipoprotein[S]Dmitry Namgaladze0Carla Jennewein1Stefan Preiss2Andreas von Knethen3Bernhard Brüne4Goethe-University, Faculty of Medicine, Institute of Biochemistry I/ZAFES, 60590 Frankfurt, GermanyGoethe-University, Faculty of Medicine, Institute of Biochemistry I/ZAFES, 60590 Frankfurt, GermanyGoethe-University, Faculty of Medicine, Institute of Biochemistry I/ZAFES, 60590 Frankfurt, GermanyGoethe-University, Faculty of Medicine, Institute of Biochemistry I/ZAFES, 60590 Frankfurt, GermanyTo whom correspondence should be addressed; Goethe-University, Faculty of Medicine, Institute of Biochemistry I/ZAFES, 60590 Frankfurt, GermanyMacrophages ingesting apoptotic cells attenuate inflammatory responses, such as reactive oxygen species (ROS) generation. In atherosclerosis, ongoing inflammation and accumulation of apoptotic/necrotic material are observed, suggesting defects of phagocytes in recognizing or responding to dying cells. Modified lipoproteins such as oxidized LDL (oxLDL) are known to promote inflammation and to interfere with apoptotic cell clearance. Here, we studied the impact of cells exposed to oxLDL on their ability to interfere with the oxidative burst in phagocytes. In contrast to apoptotic cells, cells dying in response to or in the presence of oxLDL failed to suppress ROS generation despite efficiently being taken up by phagocytes. In addition, apoptotic cells, but not oxLDL-treated cells, inhibited phosphorylation of extracellular signal-regulated kinase, which is important for NADPH oxidase activation. oxLDL treatment did not interfere with activation of the antiinflammatory transcriptional regulator peroxisome proliferator-activated receptor γ by apoptotic cells. Moreover, cells exposed to oxLDL failed to suppress lipopolysaccharide- induced proinflammatory cytokine expression, whereas apoptotic cells attenuated these phagocyte responses. Thus, the presence of oxLDL during cell death impaired the ability of apoptotic cells to act antiinflammatory with regard to oxidative burst inhibition and cytokine expression in phagocytes.http://www.sciencedirect.com/science/article/pii/S0022227520306830apoptosismacrophagesNADPH oxidaselipoproteinsphagocytosisreactive oxygen species
spellingShingle Dmitry Namgaladze
Carla Jennewein
Stefan Preiss
Andreas von Knethen
Bernhard Brüne
Attenuated suppression of the oxidative burst by cells dying in the presence of oxidized low density lipoprotein[S]
Journal of Lipid Research
apoptosis
macrophages
NADPH oxidase
lipoproteins
phagocytosis
reactive oxygen species
title Attenuated suppression of the oxidative burst by cells dying in the presence of oxidized low density lipoprotein[S]
title_full Attenuated suppression of the oxidative burst by cells dying in the presence of oxidized low density lipoprotein[S]
title_fullStr Attenuated suppression of the oxidative burst by cells dying in the presence of oxidized low density lipoprotein[S]
title_full_unstemmed Attenuated suppression of the oxidative burst by cells dying in the presence of oxidized low density lipoprotein[S]
title_short Attenuated suppression of the oxidative burst by cells dying in the presence of oxidized low density lipoprotein[S]
title_sort attenuated suppression of the oxidative burst by cells dying in the presence of oxidized low density lipoprotein s
topic apoptosis
macrophages
NADPH oxidase
lipoproteins
phagocytosis
reactive oxygen species
url http://www.sciencedirect.com/science/article/pii/S0022227520306830
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AT stefanpreiss attenuatedsuppressionoftheoxidativeburstbycellsdyinginthepresenceofoxidizedlowdensitylipoproteins
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