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Biofilms Protect Mycoplasma pulmonis Cells from Lytic Effects of Complement and Gramicidin

机译:生物膜可保护肺炎支原体细胞免受补体和葛米素的裂解作用

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The length of the tandem repeat region of the Vsa protein of Mycoplasma pulmonis has previously been shown to modulate the susceptibility of mycoplasmas to killing by complement: cells that produce a short form of the Vsa protein are highly sensitive, and cells producing the long Vsa protein are resistant. In contrast to their differing susceptibilities to complement, the mycoplasmas were highly sensitive to gramicidin irrespective of the length of the Vsa protein produced. We show here that when encased within a biofilm, cells of M. pulmonis producing a short form of the Vsa protein were more resistant to complement and gramicidin than mycoplasmas that were dispersed. The resistance appeared to be localized to those mycoplasmas within tower structures of the biofilms. Biofilm formation may be a mechanism that protects mycoplasmas from host immunity.
机译:先前已显示肺炎支原体的Vsa蛋白的串联重复序列的长度可调节支原体对补体杀伤的敏感性:产生短型Vsa蛋白的细胞高度敏感,产生长Vsa蛋白的细胞具有抗性。与补体的敏感性不同,支原体对短杆菌肽高度敏感,而与产生的Vsa蛋白长度无关。我们在这里显示,当包裹在生物膜中时, M细胞。产生短形式的Vsa蛋白的肺炎支原体比分散的支原体更耐补体和短杆菌肽。耐药性似乎局限于生物膜塔结构内的那些支原体。生物膜的形成可能是保护支原体免受宿主免疫的机制。

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