Pathogenic Yersinia enterocolitica strains increase the outer membrane permeability in response to environmental stimuli by modulating lipopolysaccharide fluidity and lipid A structure
Pathogenic Yersinia enterocolitica strains increase the outer membrane permeability in response to environmental stimuli by modulating lipopolysaccharide fluidity and lipid A structure
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DOI：
10.1128/iai.71.4.2014-2021.2003
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发表时间：
2003-04-01
影响因子：
3.1
通讯作者：
Moriyón, I
中科院分区：
文献类型：
--
作者：
Bengoechea, JA;Brandenburg, K;Moriyón, I
小肠结肠炎耶尔森氏菌的致病生物型（血清型O：3，O：8，O：9和0：13），但不是环境生物型（血清型O：5，O：6，O：7，8和O：7，8，13，19），增加了它们的渗透性疏水探针时，他们生长在pH 5.5或EGTA补充（钙2+限制）媒体在37 ℃。当血清型O：8和O：5的代表性菌株与人单核细胞短暂接触后进行检测时，也得到了类似的观察结果。渗透性的增加与毒力质粒无关。用Y.小肠结肠炎血清型O：8。在酸性或EGTA补充肉汤中生长的细菌的LPS聚集体比在标准肉汤中生长的细菌的LPS聚集体吸收更多的N-苯基萘胺，并且还显示出与渗透性相关的酰基链流动性的显著增加，如通过在疏水染料的存在下获得的测量所确定的。没有观察到O-抗原聚合的显着变化，但脂质A酰化的变化取决于生长条件。在37 ℃的标准培养基中，有六-，五-和四酰基脂质A形式，五酰基形式占主导地位。四酰基脂质A的量增加EGTA补充和酸性介质中，和六酰基脂质A几乎消失后的条件下。我们的结果表明致病性Y.小肠结肠炎菌菌株调节脂质A酰化与毒力蛋白的表达协调，从而减少LPS包装并增加外膜渗透性。在致病性Y.小肠结肠炎菌株的特征与假结核耶尔森氏菌和鼠疫耶尔森氏菌的特征相似，并表明存在与致病性相关的共同外膜模式。
Pathogenic biotypes of Yersinia enterocolitica (serotypes O:3, O:8, O:9, and 0:13), but not environmental biotypes (serotypes O:5, O:6, O:7,8, and O:7,8,13,19), increased their permeability to hydrophobic probes when they were grown at pH 5.5 or in EGTA-supplemented (Ca2+-restricted) media at 37 degreesC. A similar observation was also made when representative strains of serotypes O:8 and O:5 were tested after brief contact with human monocytes. The increase in permeability was independent of the virulence plasmid. The role of lipopolysaccharide (LPS) in this phenomenon was examined by using Y. enterocolitica serotype O:8. LPS aggregates of bacteria grown in acidic or EGTA-supplemented broth took up more N-phenylnaphthylamine than LPS aggregates of bacteria grown in standard broth and also showed a marked increase in acyl chain fluidity which correlated with permeability, as determined by measurements obtained in the presence of hydrophobic dyes. No significant changes in O-antigen polymerization were observed, but lipid A acylation changed depending on the growth conditions. In standard medium at 37 degreesC, there were hexa-, penta-, and tetraacyl lipid A forms, and the pentaacyl form was dominant. The amount of tetraacyl lipid A increased in EGTA-supplemented and acidic media, and hexaacyl lipid A almost disappeared under the latter conditions. Our results suggest that pathogenic Y. enterocolitica strains modulate lipid A acylation coordinately with expression of virulence proteins, thus reducing LPS packing and increasing outer membrane permeability. The changes in permeability, LPS acyl chain fluidity, and lipid A acylation in pathogenic Y. enterocolitica strains approximate the characteristics in Yersinia pseudotuberculosis and Yersinia pestis and suggest that there is a common outer membrane pattern associated with pathogenicity.