RI-B-NT Research Institute of Bioinformatics and Nanotechnology,Franziusallee 177, 24148 Kiel,Germany.
Department of Chemical and Biological Engineering,Chalmers University of Technology,41296 Gothenburg,Sweden.
Q Rev Biophys. 2017 Jan;50:e9. doi: 10.1017/S0033583517000075.
Interactions between human lysozyme (HL) and the lipopolysaccharide (LPS) of Klebsiella pneumoniae O1, a causative agent of lung infection, were identified by surface plasmon resonance. To characterize the molecular mechanism of this interaction, HL binding to synthetic disaccharides and tetrasaccharides representing one and two repeating units, respectively, of the O-chain of this LPS were studied. pH-dependent structural rearrangements of HL after interaction with the disaccharide were observed through nuclear magnetic resonance. The crystal structure of the HL-tetrasaccharide complex revealed carbohydrate chain packing into the A, B, C, and D binding sites of HL, which primarily occurred through residue-specific, direct or water-mediated hydrogen bonds and hydrophobic contacts. Overall, these results support a crucial role of the Glu35/Asp53/Trp63/Asp102 residues in HL binding to the tetrasaccharide. These observations suggest an unknown glycan-guided mechanism that underlies recognition of the bacterial cell wall by lysozyme and may complement the HL immune defense function.
通过表面等离子体共振,鉴定了人溶菌酶(HL)与肺炎克雷伯菌 O1 脂多糖(LPS)之间的相互作用,肺炎克雷伯菌 O1 是肺部感染的病原体。为了阐明这种相互作用的分子机制,研究了 HL 与分别代表该 LPS O 链一个和两个重复单元的合成二糖和四糖的结合。通过核磁共振观察到 HL 在与二糖相互作用后,pH 值依赖性的结构重排。HL-四糖复合物的晶体结构揭示了碳水化合物链包装到 HL 的 A、B、C 和 D 结合位点,这主要是通过残基特异性的直接或水介导氢键和疏水接触来实现的。总的来说,这些结果支持了 Glu35/Asp53/Trp63/Asp102 残基在 HL 与四糖结合中的关键作用。这些观察结果表明,溶菌酶识别细菌细胞壁的背后存在一个未知的聚糖引导机制,这可能补充了溶菌酶的免疫防御功能。