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首页> 外文期刊>Infection and immunity >Selective pressures and lipopolysaccharide subunits as determinants of resistance of clinical isolates of gram-negative bacilli to human serum.
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Selective pressures and lipopolysaccharide subunits as determinants of resistance of clinical isolates of gram-negative bacilli to human serum.

机译：选择性压力和脂多糖亚基决定了革兰氏阴性细菌对人血清的临床分离株的耐药性。

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摘要

Differences in molecular composition of lipopolysaccharides (LPS) between serum-sensitive (S) clinical isolates of Escherichia coli and serum-resistant (R) clones derived by serial passage in serum were demonstrated to determine sensitivity or resistance to killing by normal human serum (NHS). LPS from R clones had a greater proportion of higher-molecular-weight, more highly O-antigen-substituted subunits than LPS from their serum S parents. Utilization of a liposomal model with inserted LPS simulating bacterial cell walls established LPS as the site of serum bactericidal action. Liposomes containing S LPS were lysed, while liposomes containing R LPS were unaffected by NHS. R and S LPS were fractionated into higher (F1)- and lower (F2)-molecular-weight fractions. Liposomes containing R LPS or the F1 fraction of S and R LPS were not lysed by serum. Liposomes containing the F2 fraction of S or R LPS were lysed by serum analogous to that observed with liposomes containing intact S LPS. These findings establish LPS to be one site of serum bactericidal activity and demonstrate that the higher-molecular-weight, highly O-antigen-substituted LPS subunits mediate resistance to killing by NHS.
机译：大肠杆菌的血清敏感（S）临床分离株与血清中连续传代的血清抗性（R）克隆之间的脂多糖（LPS）分子组成差异被证明可确定对正常人血清（NHS）杀伤的敏感性或抗性）。与来自其血清S亲本的LPS相比，来自R克隆的LPS具有更高比例的更高分子量，更高O-抗原取代的亚基。使用具有模拟细菌细胞壁的插入LPS的脂质体模型将LPS建立为血清杀菌作用的位点。裂解含有S LPS的脂质体，而含有R LPS的脂质体不受NHS的影响。将R和S LPS分为较高（F1）-和较低（F2）分子量的馏分。血清不裂解含有R LPS或S和R LPS的F1分数的脂质体。类似于用含有完整的S LPS的脂质体观察到的，用血清裂解含有S或R LPS的F2级分的脂质体。这些发现使LPS成为血清杀菌活性的一个位点，并证明较高分子量，高O-抗原取代的LPS亚基介导了对NHS杀伤的抗性。

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