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Apoptotic cells as sources for biologically active oxidized phospholipids
Alexandra Kadl1, Valery N Bochkov, Joakim Huber
1Department of Vascular Biology and Thrombosis Research, Medical University of Vienna, Vienna, Austria.
Antioxidants & Redox Signaling
|March 18, 2004
Summary
Oxidized phospholipids from apoptotic cells propagate chronic inflammation and aid in resolving acute inflammation. These lipid oxidation products play dual roles in inflammatory processes.
Area of Science:
- Biochemistry
- Immunology
- Cell Biology
Background:
- Acute inflammation involves polymorphonuclear cell (PMN) accumulation, apoptosis, and clearance by macrophages.
- Oxidation of membrane phospholipids, particularly phosphatidylserine, occurs during apoptosis.
- Apoptotic cells release membrane vesicles containing biologically active oxidized phospholipids.
Purpose of the Study:
- To review the dual role of oxidized phospholipids generated during apoptosis.
- To discuss their involvement in propagating chronic inflammation, such as atherosclerosis.
- To explore their contribution to the resolution of acute inflammation.
Main Methods:
- Literature review of studies on oxidized phospholipids and inflammation.
- Analysis of mechanisms by which oxidized phospholipids influence inflammatory gene expression.
- Examination of the role of oxidized phospholipids in cellular signaling pathways.
Main Results:
- Oxidized phospholipids can induce pro-inflammatory genes (e.g., MCP-1, IL-8), contributing to chronic inflammatory diseases like atherosclerosis.
- These compounds exhibit anti-endotoxin effects, inhibiting lipopolysaccharide signaling.
- Oxidized phospholipids induce genes like heme oxygenase-1, crucial for acute inflammation resolution.
- They act as recognition signals, facilitating the phagocytosis of apoptotic cells.
Conclusions:
- Oxidized phospholipids generated from apoptotic cells have a dichotomous role in inflammation.
- They can propagate chronic inflammatory conditions.
- They also actively contribute to the resolution of acute inflammatory responses.