Abstract
The aim of this study was to investigate the effects of interferon-γ and -β (IFN-γ, -β), interleukin-4 and -10 (IL-4, -10) and Hpopolysaccharide (LPS) on the metabolism and composition of phospholipid fatty acids in macrophages. Murine J774.2 macrophages were incubated with radiolabelled fatty acids and the appropriate stimulus and the incorporation and composition of the phospholipid classes was determined. IFN-γ and IL-4 specifically stimulated enhanced incorporation of [14C]-linoleic acid into the phosphatidytethanolamine fraction. IL-4 (in contrast to IFN-γ and LPS) reduced incorporation of [14C]- arachidonic acid into phosphatidylinositol. Incubation of J774.2 cells with linoleic acid significantly increased TNFα and nitric oxide production; arachidonic acid enhanced TNFα production but reduced nitric oxide production. It is concluded that IFN-γ, IL-4 and IL-10 may differentially regulate macrophage activation via effects on the metabolism of polyunsaturated fatty acids.
Highlights
Bacterial endotoxin is an important inducer of the sepsis syndrome, a rapidly fatal illness which remains a major cause of morbidity and mortality in the modern medical centre
Animal models of endotoxic shock have revealed that concomitant bacterial or mycobacterial infections greatly increase susceptibility to the lethal effects of endotoxin and that antibody to tumour necrosis factor-0t (TNF00 or interferonq, (IFN-T) are beneficial.[2], It is becoming increasingly clear that IFN-T is an important mediator of hypersensitivity to endotoxin
It is believed that this could be a possible mechanism of endotoxin sensitivity and we have demonstrated that IFN-T and exogenous polyunsaturated fatty acids increase binding of LPS to mouse macrophages
Summary
Bacterial endotoxin (lipopolysaccharide, LPS) is an important inducer of the sepsis syndrome, a rapidly fatal illness which remains a major cause of morbidity and mortality in the modern medical centre. Animal models of endotoxic shock have revealed that concomitant bacterial or mycobacterial infections greatly increase susceptibility to the lethal effects of endotoxin and that antibody to tumour necrosis factor-0t (TNF00 or interferonq, (IFN-T) are beneficial.[2], It is becoming increasingly clear that IFN-T is an important mediator of hypersensitivity to endotoxin. Macrophages are primary target cells for endotoxin and by production of endogenous mediators such as superoxide anion, nitric oxide, cytokines (interleukin-1, -6, -8 (IL-1, -6, -8) and TNF) and lipid mediators (for example, prostaglandins and leukotrienes), contribute to the pathophysiology of endotoxic shock
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