Lipooligosaccharide-deficient Neisseria meningitidis shows altered pilus-associated characteristics
Lipooligosaccharide-deficient Neisseria meningitidis shows altered pilus-associated characteristics
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DOI：
10.1128/iai.71.1.155-162.2003
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发表时间：
2003-01-01
影响因子：
3.1
通讯作者：
Jonsson, AB
中科院分区：
文献类型：
--
作者：
Albiger, B;Johansson, L;Jonsson, AB
宿主粘膜表面和微生物外膜成分之间的分子相互作用在感染过程中至关重要。致病性奈瑟氏菌的外膜含有表面分子如皮利、PilC和Opa以及单层脂寡糖（LOS），所有这些都参与与宿主细胞的相互作用。皮利介导细菌最初附着于人上皮细胞，随后细菌与真核细胞紧密接触，导致细菌侵入。为了进一步研究细菌-宿主细胞接触的基础，我们构建了LOS缺陷型脑膜炎奈瑟菌血清群C突变体。LOS缺陷无一例外地伴随着改变的菌落不透明度和形态，这最有可能代表Opa 540表达的“开启”开关，以及铁调节蛋白FetA和FbpA水平的降低。我们在这里表明，LOS是必不可少的菌毛相关的粘附，但纤维的形成和抽搐的运动性。没有附着上皮细胞不能归因于改变的水平的毛或缺陷的菌毛粘附表型。此外，LOS突变体不侵入宿主细胞，并且已经失去了遗传转化的天然能力。
Molecular interaction between host mucosal surfaces and outer membrane components of microbes is crucial in the infection process. The outer membrane of pathogenic Neisseria contains surface molecules such as pili, PilC, and Opa and a monolayer of lipooligosaccharide (LOS), all of which are involved in the interaction with host cells. Pili mediate the initial attachment to human epithelial cells, which is followed by tight contact between bacteria and the eucaryotic cells, leading to bacterial invasion. To further examine the basis for bacterium-host cell contact, we constructed an LOS-deficient Neisseria meningitidis serogroup C mutant. LOS deficiency was without exception accompanied by altered colony opacity and morphology, which most likely represented an "on" switch for Opa540 expression, and by reduced levels of the iron-regulated proteins FetA and FbpA. We show here that LOS is essential for pilus-associated adherence but dispensable for fiber formation and twitching motility. The absence of attachment to epithelial cells could not be attributed to altered levels of piliation or defects in the pilus adhesion phenotype. Further, LOS mutants do not invade host cells and have lost the natural competence for genetic transformation.