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[The mechanism of macrophage apoptosis induced by lipopolysaccharide in mice]
1Department of Pathophysiology, Hunan Medical University, Changsha 410078.
Abstract:
Apoptosis is a major form of cell death, characterized morphologically by chromatin condensation and biochemically by endonuclease cleavage of DNA into oligonucleosomal fragments. We investigated apoptosis mechanism of peritoneal macrophage(M phi) induced by peritoneal injection of lipopolysaccharide(LPS) in mice. The results showed that: LPS induced the apoptosis of peritoneal M phi and concomitant decrease of phagocytosis(vs control group, P < 0.01), the concentration of NO2-/No3- in the peritoneal lavage fluid significantly increased after LPS injection; AG(inhibitor of iNOS) and PDTC(inhibitor of reactive oxygen species) prevented the apoptosis of M phi and reduced the concentration of NO2-/NO3- in the peritoneal lavage fluid. In vitro experiment, we found that AG and PDTC inhibited the apoptosis of M phi induced by IFN(100 U.ml-1) + LPS (10 micrograms.ml-1) by using DNA gel electrophoresis analysis. These evidences support that NO and active oxygen species may be involved in the apoptosis process of peritoneal M phi induced by LPS in mice.
Insights
Lipopolysaccharide (LPS) triggers apoptosis in mouse peritoneal macrophages, reducing phagocytosis. Nitric oxide (NO) and reactive oxygen species (ROS) appear to mediate this LPS-induced cell death.
Area of Science:
- Immunology
- Cell Biology
- Biochemistry
Context:
- Apoptosis, or programmed cell death, is crucial for tissue homeostasis.
- Peritoneal macrophages play a key role in innate immunity.
- Lipopolysaccharide (LPS) is a potent immune activator found in bacterial cell walls.
Purpose:
- To elucidate the mechanism of apoptosis in mouse peritoneal macrophages induced by LPS.
- To investigate the role of nitric oxide (NO) and reactive oxygen species (ROS) in LPS-induced macrophage apoptosis.
Summary:
- Peritoneal injection of LPS in mice induced apoptosis of peritoneal macrophages (M phi), accompanied by decreased phagocytosis and increased NO2-/NO3- levels.
- Inhibitors of inducible nitric oxide synthase (iNOS) and ROS, specifically AG and PDTC respectively, prevented LPS-induced M phi apoptosis.
- In vitro studies confirmed that AG and PDTC inhibited IFN + LPS-induced M phi apoptosis, suggesting NO and ROS involvement.
Impact:
- Provides mechanistic insights into LPS-induced macrophage apoptosis.
- Highlights the potential roles of NO and ROS as mediators in this process.
- Suggests potential therapeutic targets for modulating immune responses involving macrophage apoptosis.
