Department of Physics, Indiana University Purdue University Indianapolis, Indianapolis, Indiana; Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana.
Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana.
Biophys J. 2014 Feb 4;106(3):598-609. doi: 10.1016/j.bpj.2013.12.036.
The engulfment function of macrophages relies on complex molecular interactions involving both lipids and proteins. In particular, the clearance of apoptotic bodies (efferocytosis) is enabled by externalization on the cell target of phosphatidylserine lipids, which activate receptors on macrophages, suggesting that (local) specific lipid-protein interactions are required at least for the initiation of efferocytosis. However, in addition to apoptotic cells, macrophages can engulf foreign bodies that vary substantially in size from a few nanometers to microns, suggesting that nonspecific interactions over a wide range of length scales could be relevant. Here, we use model lipid membranes (made of phosphatidylcholine, phosphatidylserine, and ceramide) and rat alveolar macrophages to show how lipid bilayer properties probed by small-angle x-ray scattering and solid-state (2)H NMR correlate with engulfment rates measured by flow cytometry. We find that engulfment of protein-free model lipid vesicles is promoted by the presence of phosphatidylserine lipids but inhibited by ceramide, in accord with a previous study of apoptotic cells. We conclude that the roles of phosphatidylserine and ceramide in phagocytosis is based, at least in part, on lipid-mediated modification of membrane physical properties, including interactions at large length scales as well as local lipid ordering and possible domain formation.
巨噬细胞的吞噬作用依赖于涉及脂质和蛋白质的复杂分子相互作用。特别是,通过将磷脂酰丝氨酸脂质外化到细胞靶标上,可以实现凋亡小体(吞噬作用)的清除,这激活了巨噬细胞上的受体,表明(局部)特定的脂质-蛋白质相互作用至少对于吞噬作用的起始是必需的。然而,除了凋亡细胞外,巨噬细胞还可以吞噬大小从几纳米到几微米不等的异物,这表明在广泛的长度尺度上的非特异性相互作用可能是相关的。在这里,我们使用模型脂质膜(由磷脂酰胆碱、磷脂酰丝氨酸和神经酰胺组成)和大鼠肺泡巨噬细胞来表明小角度 X 射线散射和固态(2)H NMR 探测的脂质双层性质如何与通过流式细胞术测量的吞噬率相关。我们发现,无蛋白模型脂质囊泡的吞噬作用受到磷脂酰丝氨酸脂质的促进,但受到神经酰胺的抑制,这与先前对凋亡细胞的研究一致。我们的结论是,磷脂酰丝氨酸和神经酰胺在吞噬作用中的作用至少部分基于脂质介导的膜物理性质的修饰,包括大长度尺度上的相互作用以及局部脂质有序化和可能的域形成。