Hubbard N E, Somers S D, Erickson K L
Department of Cell Biology and Human Anatomy, School of Medicine, University of California, Davis 95616.
J Leukoc Biol. 1991 Jun;49(6):592-8. doi: 10.1002/jlb.49.6.592.
Inflammatory macrophages from mice fed diets containing menhaden fish oil (MFO) have a reduced capacity for cytotoxicity of mastocytoma cells upon activation with interferon-gamma (IFN gamma) and lipopolysaccharide due to an altered responsiveness to IFN gamma. In an effort to elucidate further how dietary MFO effects macrophage function, we have studied the maturation of inflammatory macrophages from mice fed MFO compared with mice fed safflower oil (SFO) using several processes that serve as markers of the activational state. No significant differences in the recruitment or percentage of peritoneal exudate cells as macrophages after thioglycollate injection and no differences in spreading, binding, or phagocytosis of sheep erythrocytes or phagocytosis of yeast by inflammatory macrophages were observed when the dietary groups were compared. However, MFO macrophages had an altered capacity for peroxide release when stimulated with unopsonized zymosan (10-200 micrograms/ml). Furthermore, to elucidate how MFO feeding could alter IFN gamma-induced responses of inflammatory macrophages, we assessed phorbol-12-myristate-13-acetate-induced hydrogen peroxide production and expression of class II MHC determinants (Ia). There were no differences between macrophages from mice fed the two diets with respect to the production of peroxide when they were preincubated with 0.1-10 U/ml of IFN gamma. However, MFO macrophages had greater peroxide production after enhancement with 100 U/ml of IFN gamma. With respect to Ia induction, the percentage of macrophages responding to IFN gamma was not altered by diet, and there were no differences in expression of Ia induced by 24 hr exposure to IFN gamma. Thus the differential effect of MFO compared with SFO is probably mediated not by an alteration in the maturation of inflammatory macrophages but rather through the alteration of IFN gamma-induced functions such as peroxide production.
用含鲱鱼油（MFO）的饲料喂养的小鼠体内的炎性巨噬细胞，在经γ干扰素（IFNγ）和脂多糖激活后，对肥大细胞瘤细胞的细胞毒性能力降低，这是由于对IFNγ的反应性改变所致。为了进一步阐明饮食中的MFO如何影响巨噬细胞功能，我们研究了用几种作为激活状态标志物的过程，比较用MFO喂养的小鼠与用红花油（SFO）喂养的小鼠体内炎性巨噬细胞的成熟情况。当比较不同饮食组时，在注射巯基乙酸盐后作为巨噬细胞的腹腔渗出细胞的募集或百分比没有显著差异，并且炎性巨噬细胞对绵羊红细胞的铺展、结合或吞噬以及对酵母的吞噬也没有差异。然而，当用未调理的酵母聚糖（10 - 200微克/毫升）刺激时，MFO巨噬细胞释放过氧化物的能力发生了改变。此外，为了阐明喂食MFO如何改变IFNγ诱导的炎性巨噬细胞反应，我们评估了佛波醇-12-肉豆蔻酸酯-13-乙酸酯诱导的过氧化氢产生和II类主要组织相容性复合体决定簇（Ia）的表达。当用0.1 - 10单位/毫升的IFNγ预孵育时，两种饮食喂养的小鼠的巨噬细胞在过氧化物产生方面没有差异。然而，在用100单位/毫升的IFNγ增强后，MFO巨噬细胞产生的过氧化物更多。关于Ia诱导，对IFNγ有反应的巨噬细胞百分比不受饮食影响，并且在暴露于IFNγ 24小时后诱导的Ia表达也没有差异。因此，与SFO相比，MFO的差异效应可能不是通过炎性巨噬细胞成熟的改变介导的，而是通过IFNγ诱导的功能如过氧化物产生的改变介导的。
