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Stimulation of peritoneal cell arginase by bacterial lipopolysaccharides
Abstract:
The conditions under which bacterial endotoxins stimulate arginase production in mouse peritoneal macrophages have been defined. Both lipid-A and lipid-A-associated protein are potent activators. Fetal calf serum and normal mouse serum enhance macrophage arginase levels in the presence and absence of lipopolysaccharide (LPS). LPS in the amount of 10(-1) microgram/ml represents a maximal stimulus for macrophage arginase production and release. Thioglycollate-elicited peritoneal cells have increased arginase activity, compared with resident cells. This activity can be stimulated further by the addition of LPS. Arginase levels may alter the outcome of in vitro immunologic processes by depleting arginine and may also serve as a useful indicator of the state of activation of macrophages.
Insights
Bacterial endotoxins, including lipid-A, strongly stimulate macrophage arginase production. This enzyme
Area of Science:
- Immunology
- Cell Biology
- Biochemistry
Background:
- Bacterial endotoxins are key immune activators.
- Macrophage activation influences immune responses.
- Arginase plays a role in cellular metabolism and immunity.
Purpose of the Study:
- To define conditions for bacterial endotoxin-induced arginase production in mouse macrophages.
- To investigate the role of lipid-A and associated proteins in this process.
- To assess the impact of serum and lipopolysaccharide (LPS) on macrophage arginase activity.
Main Methods:
- Primary culture of mouse peritoneal macrophages.
- Stimulation with bacterial endotoxin components (lipid-A, lipid-A-associated protein).
- Treatment with fetal calf serum, mouse serum, and lipopolysaccharide (LPS).
- Measurement of arginase activity in macrophages.
Main Results:
- Lipid-A and lipid-A-associated protein are potent stimulators of arginase production.
- Fetal calf serum and normal mouse serum enhance basal and LPS-induced arginase levels.
- Lipopolysaccharide (LPS) at 10(-1) microgram/ml is a maximal stimulus for arginase production and release.
- Thioglycollate-elicited macrophages exhibit higher arginase activity than resident cells, further enhanced by LPS.
Conclusions:
- Bacterial endotoxins, particularly lipid-A, effectively induce arginase production in macrophages.
- Serum components and LPS significantly modulate macrophage arginase levels.
- Arginase activity in macrophages can be a marker of cellular activation and may impact immune processes by arginine depletion.