PNAS:流感继发细菌性肺炎研究获进展

2015-01-09 张章 科学网

流感是历史上造成人类死亡最多的疾病之一,而其中约90%的死亡病例的死因是继发细菌性肺炎。中科院微生物研究所王北难课题组日前在美国《国家科学院院刊》发表最新研究结果,揭示了病毒和细菌与宿主在致病机制中的相互关系,以及流感病毒与细菌性肺炎相关的分子机制,为预防细菌性肺炎和控制流感死亡率提供了不同的角度和新药物靶点。 据介绍,虽然流感病毒继发的肺部细菌感染现象被人们广泛关注,但其分子机制仍不清

流感是历史上造成人类死亡最多的疾病之一,而其中约90%的死亡病例的死因是继发细菌性肺炎。中科院微生物研究所王北难课题组日前在美国《国家科学院院刊》发表最新研究结果,揭示了病毒和细菌与宿主在致病机制中的相互关系,以及流感病毒与细菌性肺炎相关的分子机制,为预防细菌性肺炎和控制流感死亡率提供了不同的角度和新药物靶点。

据介绍,虽然流感病毒继发的肺部细菌感染现象被人们广泛关注,但其分子机制仍不清楚。为了控制流感暴发引起细菌性肺炎而造成的死亡,了解其机制是重要前提。

王北难课题组发现,流感病毒的神经氨酸酶(NA)可以活化宿主体内的转化生长因子-β(TGF-β),导致宿主细胞表面的黏附分子表达增高。此类黏附分子(例如纤连蛋白和整合素)与细菌黏附宿主细胞表面相关,会使细菌对宿主肺细胞的黏附增加,从而引起继发的细菌感染,而抑制病毒NA的活性或TGF-β信号传导通路就能有效地阻断流感病毒感染后细菌对肺组织的黏附。

该研究小组还证明,流感病毒介导的细菌黏附由细菌表面的纤维蛋白结合蛋白引起,因此拥有该类毒力蛋白的细菌与流感继发的细菌感染密切相关,例如肺炎球菌、金黄色葡萄球菌、A型链球球菌和流感嗜血杆菌。

原始出处:

Li N1, Ren A1, Wang X1, Fan X1, Zhao Y2, Gao GF1, Cleary P3, Wang B4.Influenza viral neuraminidase primes bacterial coinfection through TGF-β-mediated expression of host cell receptors.Proc Natl Acad Sci U S A. 2015 Jan 6;112(1):238-43. doi: 10.1073/pnas.1414422112. Epub 2014 Dec 22.

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    2015-10-10 drwjr
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    2015-03-31 feifers
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PNAS:中科院发现流感容易引发肺炎的分子机制

流感病毒感染之后会让宿主更容易患上细菌性肺炎。这种共感染(coinfection)现象也是流感大流行时造成患者死亡的主要原因。然而,人们此前并不清楚这种现象背后的具体分子机制。中科院微生物研究所的研究团队发现,甲型流感病毒(IAV)的神经氨酸酶(NA)能够通过激活TGF-β上调粘附分子(比如纤连蛋白和整合蛋白)的表达,帮助致病菌粘附在宿主细胞上。这一成果发表在近期的美国国家科学院院刊PNA