Removal of the outer Kdo from Helicobacter pylori lipopolysaccharide and its impact on the bacterial surface.
Removal of the outer Kdo from Helicobacter pylori lipopolysaccharide and its impact on the bacterial surface.
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DOI：
10.1111/j.1365-2958.2010.07304.x
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发表时间：
2010-11
影响因子：
3.6
通讯作者：
Trent MS
中科院分区：
文献类型：
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作者：
Stead CM;Zhao J;Raetz CR;Trent MS
幽门螺杆菌产生一种独特的表面脂多糖（LPS），其特点是内毒性非常低，被认为有助于生物体逃避宿主的免疫反应。内毒性的降低预计是由一系列膜结合酶修饰幽门螺杆菌LPS的Kdo-脂质A结构域引起的，包括负责修饰核心低聚糖的Kdo（3-脱氧-d -甘露糖醛酸）水解酶。在这里，我们报道Kdo水解酶的活性依赖于一个假定的由Hp0579和Hp0580组成的两蛋白复合物。Kdo水解酶活性失活产生两种与阳离子抗菌肽（CAMP）抗性和o抗原表达相关的表型。Kdo水解酶突变体对多粘菌素B高度敏感，这可能归因于脂质4a ' -磷酸基团下游修饰的缺陷。在Kdo水解酶突变体中，完全延伸的o型抗原的产生也减少，从而导致核心脂质a的增加。最后，o型抗原Lewis X和Y表位的表达也受到影响，这些表位可以模拟人体组织中的糖缀合物。综上所述，我们已经证明Kdo水解酶活性的丧失影响了幽门螺杆菌LPS的所有三个结构域，从而突出了它在维持细菌表面中的作用。
Helicobacter pylori produces a unique surface lipopolysaccharide (LPS) characterized by strikingly low endotoxicity that is thought to aid the organism in evading the host immune response. This reduction in endotoxicity is predicted to arise from the modification of the Kdo-lipid A domain of Helicobacter LPS by a series of membrane bound enzymes including a Kdo (3-deoxy-D-manno-octulosonic acid) hydrolase responsible for the modification of the core-oligosaccharide. Here we report that Kdo hydrolase activity is dependent upon a putative two-protein complex composed of proteins Hp0579 and Hp0580. Inactivation of Kdo hydrolase activity produced two phenotypes associated with cationic antimicrobial peptide (CAMP) resistance and O-antigen expression. Kdo hydrolase mutants were highly sensitive to polymyxin B, which could be attributed to a defect in downstream modifications to the lipid A 4′-phosphate group. Production of a fully extended O-antigen was also diminished in a Kdo hydrolase mutant, with a consequent increase in core-lipid A. Finally, expression of O-antigen Lewis X and Y epitopes, known to mimic glycoconjugates found on human tissues, was also affected. Taken together, we have demonstrated that loss of Kdo hydrolase activity affects all three domains of H. pylori LPS, thus highlighting it’s role in the maintenance of the bacterial surface.
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影响因子：
3.6
作者：
Gunn, JS;Lim, KB;Miller, SI
通讯作者：
Miller, SI
影响因子：
2.2
作者：
LESSE, AJ;CAMPAGNARI, AA;APICELLA, MA
通讯作者：
APICELLA, MA
DOI：
10.1073/pnas.93.25.14648
发表时间：
1996-12-10
影响因子：
11.1
作者：
Censini, S;Lange, C;Covacci, A
通讯作者：
Covacci, A
影响因子：
4.8
作者：
Kaniuk, NA;Vinogradov, E;Whitfield, C
通讯作者：
Whitfield, C
大肠杆菌K-12的构造框架，单基因敲除突变体：Keio Collection。
影响因子：
9.9
作者：
通讯作者：
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