Srimal S, Surolia N, Balasubramanian S, Surolia A
Molecular Biophysics Unit, Indian Institute of Science, Bangalore, India.
Biochem J. 1996 Apr 15;315 ( Pt 2)(Pt 2):679-86. doi: 10.1042/bj3150679.
Lipopolysaccharide (LPS), the major cell wall constituent of Gram-negative bacteria, evokes a multitude of biological effects in mammals including pyrogenicity and toxic shock syndrome. Polymyxin B (PmB), a polycationic cyclic peptide, is known to neutralize most of its activities. The nature of the interaction of PmB with LPS and lipid A was investigated by isothermal titration calorimetry. PmB binds to LPS as well as lipid A stoichiometrically and non-co-operatively with micromolar affinity. These interactions are driven primarily by a favourable change in entropy (delta S) and are endothermic in nature. These positive changes in enthalpies decrease with increasing temperature, yielding a heat capacity change, delta Cp, of -2385 J.mol-1.degree-1 for PmB-LPS interactions while the binding of PmB to lipid A displays a delta Cp of -2259 J.mol-1.degree-1. The negative heat capacity changes provide strong evidence for the role of hydrophobic interactions as the driving force for the association of PmB with LPS and lipid A. A correlation of the energetics of these interactions with analyses of the molecular models of PmB suggests that a cluster of solvent-exposed non-polar amino acid side-chains that line one surface of the molecule, together with a ring of positively charged residues on its other surface, are responsible for its strong and stoichiometric binding to LPS.
脂多糖(LPS)是革兰氏阴性菌细胞壁的主要成分,可在哺乳动物中引发多种生物学效应,包括发热性和中毒性休克综合征。多粘菌素B(PmB)是一种聚阳离子环肽,已知可中和其大部分活性。通过等温滴定量热法研究了PmB与LPS和脂质A的相互作用性质。PmB以化学计量方式且非协同地与LPS以及脂质A结合,亲和力为微摩尔级。这些相互作用主要由熵的有利变化(ΔS)驱动,本质上是吸热的。随着温度升高,这些焓的正向变化减小,PmB-LPS相互作用的热容变化ΔCp为-2385 J·mol⁻¹·℃⁻¹,而PmB与脂质A的结合显示ΔCp为-2259 J·mol⁻¹·℃⁻¹。负的热容变化为疏水相互作用作为PmB与LPS和脂质A结合的驱动力这一作用提供了有力证据。这些相互作用的能量学与PmB分子模型分析之间的相关性表明,分子一个表面排列的一簇溶剂暴露的非极性氨基酸侧链,以及其另一个表面的带正电荷残基环,负责其与LPS的强化学计量结合。