Pneumococcal neuraminidase A: an essential upper airway colonization factor for Streptococcus pneumoniae
Pneumococcal neuraminidase A: an essential upper airway colonization factor for Streptococcus pneumoniae
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DOI：
10.1111/j.2041-1014.2012.00658.x
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发表时间：
2012-08-01
影响因子：
3.7
通讯作者：
Jenkinson, H. F.
中科院分区：
文献类型：
--
作者：
Brittan, J. L.;Buckeridge, T. J.;Jenkinson, H. F.
肺炎链球菌在上呼吸道定居，从那里微生物可能会系统性传播，导致危及生命的感染。肺炎球菌定植上皮细胞的机制尚不清楚，但神经氨酸酶A(NANA)在促进上呼吸道的生长和存活方面起着重要作用。在本文中，我们发现与肺炎链球菌D39相似的突变株缺乏NaNA或神经氨酸酶B(NanB)，它们与三种上皮细胞株和原代鼻咽细胞的粘附性被取消。在反式中，Nana互补可部分恢复依从性水平。NaNA的酶活性是肺炎球菌与上皮细胞黏附所必需的，通过将表达NaNA的乳球菌细胞与上皮细胞预先孵育，可将其黏附恢复到野生型水平。肺炎链球菌的nana或nanB突变体缺乏生物被膜的形成，而与乳酸或戈登链球菌相似的L.这些结果表明，NaNA是一种酶因子，通过破译黏附受体来调节与上皮细胞的黏附，并且至少部分地作为生物膜形成中的粘附素发挥作用。因此，神经氨酸酶A似乎在肺炎球菌感染中扮演着多个暂时性的角色，从附着宿主组织、定植和社区发展，到全身扩散和跨越血脑屏障。
Streptococcus pneumoniae colonizes the upper respiratory tract from where the organisms may disseminate systemically to cause life threatening infections. The mechanisms by which pneumococci colonize epithelia are not understood, but neuraminidase A (NanA) has a major role in promoting growth and survival in the upper respiratory tract. In this article we show that mutants of S.similar to pneumoniae D39 deficient in NanA or neuraminidase B (NanB) are abrogated in adherence to three epithelial cell lines, and to primary nasopharyngeal cells. Adherence levels were partly restored by nanA complementation in trans. Enzymic activity of NanA was shown to be necessary for pneumococcal adherence to epithelial cells, and adherence of the nanA mutant was restored to wild-type level by pre-incubation of epithelial cells with Lactococcus lactis cells expressing NanA. Pneumococcal nanA or nanB mutants were deficient in biofilm formation, while expression of NanA on L.similar to lactis or Streptococcus gordonii promoted biofilm formation by these heterologous host organisms. The results suggest that NanA is an enzymic factor mediating adherence to epithelial cells by decrypting receptors for adhesion, and functions at least in part as an adhesin in biofilm formation. Neuraminidase A thus appears to play multiple temporal roles in pneumococcal infection, from adherence to host tissues, colonization, and community development, to systemic spread and crossing of the blood-brain barrier.