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Molecular and Structural Damage to Escherichia coli Produced by Antibody Complement and Lysozyme Systems

机译:抗体补体和溶菌酶系统对大肠杆菌的分子和结构损伤

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摘要

The antibacterial action of antibody (normal and hyperimmune), complement, and lysozyme has been studied by correlating the ultrastructural and biochemical changes that they cause in smooth Escherichia coli. Both normal and hyperimmune antibody, in the absence of lysozyme, produced complement-dependent release, into the suspending medium, of 63 to 72% of the 32P-labeled phospholipid and 74 to 85% of the small molecular bacterial constituents. Macromolecular nucleic acid labeled with 32P was not released. By phase microscopy, these cells appeared as bacilli but their ultrastructure showed general swelling, with smoothing of the normally wrinkled outer cell wall layers. Cytoplasmic membranes were damaged and the internal cell structure was disorganized. Membranous spherules, apparently from the outermost putatively lipopolysaccharide cell layer, were released into the medium. When lysozyme was added to antibody and complement, 32P-labeled macromolecular constituents were released from the cells. Damage to ultrastructure then included loss of cell wall rigidity, cell wall breakage, and some spheroplast formation. Characteristic fibrillar fragmentation was seen in cell wall mucopeptide layers. The relationships between antibody-complement dependent release of bacterial phospholipid, loss of selective cell permeability, and increase in sensitivity to lysozyme are discussed.
机译:通过关联在平滑大肠杆菌中引起的超微结构和生化变化,研究了抗体(正常和超免疫),补体和溶菌酶的抗菌作用。在没有溶菌酶的情况下,正常抗体和超免疫抗体都会产生补体依赖性释放到悬浮介质中的 32 P标记的磷脂中的63%至72%,以及小剂量的74%至85%分子细菌成分。 32 P标记的大分子核酸未释放。通过相显微镜,这些细胞表现为杆菌,但是它们的超微结构显示出一般的肿胀,并且平滑了通常起皱的细胞外壁层。细胞质膜受损,内部细胞结构混乱。显然来自最外层的脂多糖细胞层的膜小球被释放到培养基中。将溶菌酶加入抗体和补体中后, 32 P标记的大分子成分从细胞中释放出来。然后,对超微结构的损害包括细胞壁刚性的丧失,细胞壁的断裂以及一些原生质球的形成。在细胞壁粘肽层中观察到特征性纤维状碎片。讨论了细菌磷脂的抗体补体依赖性释放,选择性细胞通透性丧失和对溶菌酶敏感性增加之间的关系。

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