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Liposomal induction of a heat-stable macrophage priming factor to induce nitric oxide in response to LPS
1School of Pharmacy, Tokyo University of Pharmacy and Life Science, Japan.
Purpose:
The effects of liposomes on nitric oxide (NO) production from mouse peritoneal macrophages following intraperitoneal injection of liposomes were investigated.
Methods:
Mouse peritoneal macrophages were collected following intraperitoneal injection of liposomes and cultured with and without lipopolysaccharide (LPS). Peritoneal washing fluid was also collected from the mice injected with liposomes. NO production was evaluated by measuring the concentration of nitrite in the macrophage culture supernatant by Griess reagent.
Results:
NO production stimulated by LPS was observed in peritoneal macrophages obtained from the liposome-treated mice, but liposomes did not active macrophages directly to induce NO in response to LPS. NO production was higher in the liposomes composed of phosphatidylcholine than that of negatively charged liposomes composed of phosphatidylserine. Peritoneal washing fluid obtained from mice injected with liposomes has a capacity to induce NO production in the macrophages from naive mice. This capacity was not diminished by heat-treatment at 100 degrees C for 5 min.
Conclusions:
Peritoneal macrophages were activated to produce NO in response to LPS following intraperitoneal injection of liposomes. They did not activate macrophages directly, and the induction of heat-stable macrophage priming factor, but not cytokines, is suggested.
Insights
Liposomes administered intraperitoneally prime mouse macrophages to produce nitric oxide (NO) in response to lipopolysaccharide (LPS). This priming effect is mediated by a heat-stable factor, not direct macrophage activation.
Area of Science:
- Immunology
- Nanomedicine
- Cell Biology
Background:
- Liposomes are versatile drug delivery systems.
- Nitric oxide (NO) plays a crucial role in immune responses.
- Macrophage activation is key to innate immunity.
Purpose of the Study:
- To investigate the impact of intraperitoneal liposome administration on nitric oxide (NO) production by mouse peritoneal macrophages.
- To determine if liposomes directly activate macrophages or induce a priming effect.
Main Methods:
- Mice received intraperitoneal liposome injections.
- Peritoneal macrophages were isolated and cultured with or without lipopolysaccharide (LPS).
- Nitrite concentration in culture supernatants was measured using the Griess reagent to assess NO production.
Main Results:
- Liposome-treated macrophages produced NO when stimulated with LPS, indicating priming.
- Liposomes did not directly activate macrophages to produce NO.
- Phosphatidylcholine liposomes induced higher NO production than phosphatidylserine liposomes.
- Peritoneal washing fluid from liposome-injected mice contained a heat-stable factor that induced NO production in naive macrophages.
Conclusions:
- Intraperitoneal liposomes prime peritoneal macrophages for LPS-induced NO production.
- The priming effect is mediated by a heat-stable factor, suggesting a non-cytokine mechanism.
- Liposomes do not directly activate macrophages but induce a state of readiness for immune response.