Triggering of the macrophage and neutrophil respiratory burst by antibody bound to a spin-label phospholipid hapten in model lipid bilayer membranes.
Triggering of the macrophage and neutrophil respiratory burst by antibody bound to a spin-label phospholipid hapten in model lipid bilayer membranes.
复制标题
通过与模型脂质双层膜中的自旋标记磷脂半抗原结合的抗体触发巨噬细胞和中性粒细胞呼吸爆发。
DOI：
10.1021/bi00564a037
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发表时间：
1980
期刊：
影响因子：
2.9
通讯作者：
McConnell,HM
中科院分区：
文献类型：
--
作者：
Hafeman,DG;Lewis,JT;McConnell,HM
1-C-葡萄糖氧化）的RAW 264巨噬细胞系的半抗原化的脂质囊泡强烈依赖于脂质膜的物理性质，以及囊泡上的抗体的表面密度。在37 ℃下为“固体”的脂质膜（二棕榈酰磷脂酰胆碱，DPPC）比“流体”膜（二肉豆蔻酰磷脂酰胆碱，DMPC）有效得多，每个囊泡结合.囊泡膜。已经报道了关于免疫系统的各种组分与含有特异性半抗原或抗原的模型膜（形成囊泡或脂质体的脂质双层）的相互作用的各种研究（Esser等，1979; Finberg等，1978;盖革和Schreiber，1979;黑尔等人，1980; Kinsky和Nicolotti，1977; Hafeman等人，1979; Henkart &布卢门塔尔，1975;亨利等人，1978;霍兰德等人，1979年;刘易斯和麦康奈尔，1978年;洛等人，1979; McConnell，1978; Parce等人，1978、1980年）。这些研究中的一些已经描述了免疫应答对宿主双层膜的物理-化学性质的依赖性（Esser等人，1979; Hafeman等人，1979年;刘易斯和麦康奈尔，1978年; Parce等人，1980; McConnell，1978）。例如，相对于“固体”DPPC膜，“流体”DMPC 1膜中补体Q的第一组分的活化和补体消耗增强（Esser等人，1979; Parce等人，1980年）。同样地，胆固醇包含在固体DPPC膜中导致补体消耗增加（Humphries & McConnell，1975; Brulet & McConnell，1977）。我们将双层膜称为“流体”或“固体”，这取决于脂质半抗原和与这些半抗原结合的抗体的横向扩散系数是> 10 - 8 cm 2/s还是< 10 - 10 cm 2/s（Smith等人，1979年）。在所附的论文（刘易斯等人，1980），我们表明，与固体DPPC囊泡相比，半抗原化脂质囊泡的特异性抗体依赖性结合的动力学在流体DMPC囊泡中同样增强，并且当胆固醇包含在DPPC囊泡中时增强。在本论文中，我们报告了这些相关性的意外逆转，发现固体半抗原化DPPC囊泡在刺激巨噬细胞系RAW 264中的呼吸爆发方面比流体DMPC囊泡（每个囊泡结合）有效得多。同样地，DPPC中包含胆固醇降低了这种呼吸爆发。因此，在识别（结合）和细胞触发中涉及明显不同的膜分子特性。
1-C-glucose oxidation) of RAW264 macrophage cell line by haptenated lipid vesicles depends strongly on the physical properties of the lipid membrane, as well as the surface density of antibodies on the vesicles. Lipid membranes that are “solid” at 37 C (dipalmitoylphosphatidylcholine, DPPC) are much more effective, per vesicle bound, than are “fluid” membranes (dimyristoylphosphatidylcholine, DMPC). Vesicle membranes.^^. t present a variety of studies have been reported on the interactions of various components of the immune system with model membranes (lipid bilayers forming vesicles or liposomes) containing specific haptens or antigens (Esser et al, 1979; Finberg et al., 1978; Geiger & Schreiber, 1979; Hale et al., 1980; Kinsky & Nicolotti, 1977; Hafeman et al., 1979; Henkart & Blumenthal, 1975; Henry et al., 1978; Hollander et al., 1979; Lewis & McConnell, 1978; Loh et al., 1979; McConnell, 1978; Parce et al., 1978, 1980). Some of these studies have described a dependence of immune response on the physical-chemical properties of the hostbilayer membranes (Esser et al., 1979; Hafeman et al., 1979; Lewis & McConnell, 1978; Parce et al., 1980; McConnell, 1978). For example, the activation of the first component of complement Q and com-plement depletion are enhanced in “fluid” DMPC1 membranes relative to “solid” DPPC membranes (Esser et al., 1979; Parce et al., 1980). Likewise the inclusion of cholesterol in otherwise solid DPPC membranesleads to an enhancement in complement depletion (Humphries & McConnell, 1975; Brulet & McConnell, 1977). We refer to bilayer membranes as “fluid” or “solid”, depending on whether the lateral diffusion coef-ficients of lipid haptens, and antibodies bound to these haptens, are> 10~ 8 cm2/s or< 10~ 10 cm2/s (Smith et al., 1979). In the accompanying paper (Lewis et al., 1980) we show that the kinetics of specific antibody-dependent binding of haptenated lipid vesicles is likewise enhanced in fluid DMPC vesicles compared to solid DPPC vesicles and is enhanced when cholesterol is included in DPPC vesicles. In the present paper we report an unexpected reversal of these correlations, in that solid haptenated DPPC vesicles are found to be far more effective than fluid DMPC vesicles (per vesicle bound) in stimulating the respiratory burst in the macrophage cell line RAW264. Likewise, inclusion of cholesterol in DPPC decreases this re-spiratory burst. Thus, markedly different membrane molecular properties are involved in recognition (binding) and in cell triggering.