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首页> 外文期刊>Infection and immunity >The (alpha2-->8)-linked polysialic acid capsule of group B Neisseria meningitidis modifies multiple steps during interaction with human macrophages.
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The (alpha2-->8)-linked polysialic acid capsule of group B Neisseria meningitidis modifies multiple steps during interaction with human macrophages.

机译：B群脑膜炎奈瑟氏球菌的（α2-→8）-连接的多唾液酸胶囊在与人巨噬细胞相互作用期间修饰了多个步骤。

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    Group B Neisseria meningitidis causes systemic disease, including meningitis, after initial colonization and subsequent penetration of nasopharyngeal mucosa, a tissue which is richly populated by macrophages. In an initial effort to characterize the interaction of N. meningitidis and mature human macrophages, the influence of the alpha2-->8) -linked polysialic acid capsule on the interaction of N. meningitidis with human monocyte-derived macrophages was investigated with a capsulate case isolate and an isogenic Tn916-derived noncapsulate transformant. The capsulate strain was fourfold less adherent to the macrophage surface after cold incubation, although adherence of both strains was significantly increased after opsonization with nonimmune C5-depleted serum. When opsonized inocula were adjusted so that they adhered to macrophages in equal numbers, the two strains were internalized at equivalent rates and both entered membrane-bound compartments (phagosomes). Colocalization of bacteria with the late endosomal and lysosomal marker lysosome-associated membrane protein revealed that fusion of lysosomes with phagosomes containing the capsulate organism was significantly reduced 10 and 30 min after entry, but by 1 h, no difference between the strains was observed. Once internalized, meningococci were effectively killed, although more rapid killing of the capsulate strain was observed over the first 3 h. These results indicate that the (alpha2-->8)-linked polysialic acid capsule modifies the interaction of meningococci with human macrophages at multiple steps, including adherence to the macrophage surface and phagosome-lysosome fusion. Moreover, the discordance between the kinetics of phagosome- lysosome fusion and bacterial killing suggests that a nonlysosomal mechanism may be responsible for a significant fraction of macrophage killing of N. meningitidis.
    机译：B组脑膜炎奈瑟氏球菌在最初定殖并随后穿透鼻咽粘膜（一种富含巨噬细胞的组织）后，引起全身性疾病，包括脑膜炎。为了表征脑膜炎奈瑟氏球菌和成熟的人类巨噬细胞之间的相互作用，我们首先研究了α2-> 8）-连接的多唾液酸胶囊对脑膜炎奈瑟氏球菌与人单核细胞衍生的巨噬细胞相互作用的影响。案例分离物和同基因的Tn916衍生的非荚膜转化体。冷培养后，荚膜菌株对巨噬细胞表面的粘附减少了四倍，尽管在用未免疫的C5贫血血清调理后，两种菌株的粘附均显着增加。调节调理剂接种物以使它们以相等数量粘附在巨噬细胞上时，两种菌株以相同的速率被内化，并且都进入膜结合区室（吞噬体）。细菌与晚期内体和溶酶体标记物溶酶体相关膜蛋白的共定位显示，进入后10和30分钟，溶酶体与含有囊状生物体的吞噬体的融合显着减少，但是到1 h，菌株之间没有发现差异。一旦内在化，脑膜炎球菌可被有效杀死，尽管在最初的3小时内观察到了更快速的荚膜菌株杀灭。这些结果表明，（α2-→8）-连接的聚唾液酸胶囊在多个步骤上改变了脑膜炎球菌与人巨噬细胞的相互作用，包括粘附于巨噬细胞表面和吞噬体-溶酶体融合。此外，吞噬-溶酶体融合动力学与细菌杀灭之间的不一致表明，非溶酶体机制可能是脑膜炎奈瑟氏球菌巨噬细胞杀伤的重要部分。

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