Henderson J Michael, Waring Alan J, Separovic Frances, Lee Ka Yee C
Department of Chemistry, The University of Chicago, Chicago, Illinois; Institute for Biophysical Dynamics, The University of Chicago, Chicago, Illinois; The James Frank Institute, The University of Chicago, Chicago, Illinois.
Los Angeles Biomedical Research Institute, Harbor-UCLA Medical Center, Torrance, California; Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California.
Biophys J. 2016 Nov 15;111(10):2176-2189. doi: 10.1016/j.bpj.2016.10.003.
Antimicrobial peptides (AMPs) are a class of host-defense molecules that neutralize a broad range of pathogens. Their membrane-permeabilizing behavior has been commonly attributed to the formation of pores; however, with the continuing discovery of AMPs, many are uncharacterized and their exact mechanism remains unknown. Using atomic force microscopy, we previously characterized the disruption of model membranes by protegrin-1 (PG-1), a cationic AMP from pig leukocytes. When incubated with zwitterionic membranes of dimyristoylphosphocholine, PG-1 first induced edge instability at low concentrations, then porous defects at intermediate concentrations, and finally worm-like micelle structures at high concentrations. These rich structural changes suggested that pore formation constitutes only an intermediate state along the route of PG-1's membrane disruption process. The formation of these structures could be best understood by using a mesophase framework of a binary mixture of lipids and peptides, where PG-1 acts as a line-active agent in lowering interfacial bilayer tensions. We have proposed that rather than being static pore formers, AMPs share a common ability to lower interfacial tensions that promote membrane transformations. In a study of 13 different AMPs, we found that peptide line-active behavior was not driven by the overall charge, and instead was correlated with their adoption of imperfect secondary structures. These peptide structures commonly positioned charged residues near the membrane interface to promote deformation favorable for their incorporation into the membrane. Uniquely, the data showed that barrel-stave-forming peptides such as alamethicin are not line-active, and that the seemingly disparate models of toroidal pores and carpet activity are actually related. We speculate that this interplay between peptide structure and the distribution of polar residues in relation to the membrane governs AMP line activity in general and represents a novel, to our knowledge, avenue for the rational design of new drugs.
抗菌肽(AMPs)是一类可中和多种病原体的宿主防御分子。它们的膜通透行为通常被认为是由孔的形成导致的;然而,随着抗菌肽的不断发现,许多抗菌肽尚未得到表征,其确切机制仍然未知。我们之前利用原子力显微镜对来自猪白细胞的阳离子抗菌肽protegrin-1(PG-1)破坏模型膜的过程进行了表征。当与二肉豆蔻酰磷脂酰胆碱的两性离子膜一起孵育时,PG-1在低浓度时首先诱导边缘不稳定,在中等浓度时诱导多孔缺陷,最终在高浓度时诱导形成蠕虫状胶束结构。这些丰富的结构变化表明,孔的形成仅仅是PG-1膜破坏过程中的一个中间状态。通过使用脂质和肽二元混合物的中间相框架,可以最好地理解这些结构的形成,其中PG-1作为一种线活性剂降低界面双层张力。我们提出,抗菌肽并非静态的孔形成剂,而是具有共同的降低界面张力的能力,从而促进膜的转变。在一项对13种不同抗菌肽的研究中,我们发现肽的线活性行为不是由整体电荷驱动的,而是与其采用的不完美二级结构相关。这些肽结构通常将带电荷的残基定位在膜界面附近,以促进有利于其融入膜的变形。独特的是,数据表明诸如短杆菌肽之类的桶状孔形成肽没有线活性,并且环形孔和地毯活性这些看似不同的模型实际上是相关的。我们推测,肽结构与极性残基相对于膜的分布之间的这种相互作用总体上决定了抗菌肽的线活性,并且据我们所知,代表了一种合理设计新药的新途径。