Chemorepulsion from the Quorum Signal Autoinducer-2 Promotes Helicobacter pylori Biofilm Dispersal.
Chemorepulsion from the Quorum Signal Autoinducer-2 Promotes Helicobacter pylori Biofilm Dispersal.
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DOI：
10.1128/mbio.00379-15
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发表时间：
2015-07-07
期刊：
影响因子：
6.4
通讯作者：
Guillemin K
中科院分区：
文献类型：
--
作者：
Anderson JK;Huang JY;Wreden C;Sweeney EG;Goers J;Remington SJ;Guillemin K
胃病原体幽门螺杆菌在非生物和生物表面形成生物膜。我们之前已经证明，幽门螺杆菌将群体信号自诱导剂 2 (AI-2) 视为化学驱避剂。我们在此报告，内源性 AI-2 产生的幽门螺杆菌化学排斥会影响生物膜内细胞的比例和空间组织。无法产生 AI-2 的菌株（ΔluxS 菌株）或趋化性有缺陷的菌株（ΔcheA 菌株）形成了空间更均匀的生物膜，与野生型生物膜相比，贴壁细胞与浮游细胞的比例更大。相反，过量产生 AI-2 (luxSOP) 的菌株形成的生物膜中贴壁细胞相对较少。除了已知的 AI-2 化学感受器 TlpB，我们还鉴定了 AibA 和 AibB，这是 AI-2 化学脉冲反应所需的两种新型周质结合蛋白。 AI-2 趋化性所需的任何蛋白质的破坏概括了 ΔluxS 突变体的生物膜粘附和空间组织表型。此外，外源施用AI-2足以降低生物膜中贴壁细胞的比例，并以趋化依赖性方式促进细胞从生物膜中分散。最后，我们发现 AI-2 产生或 AI-2 趋化性的破坏导致培养的上皮细胞上微集落中的细胞聚集增加。我们得出的结论是，AI-2 的趋化性是幽门螺杆菌生物膜空间组织和扩散的决定因素。细菌生物膜在自然界中无处不在，但其组装和空间组织的机制尚不完全清楚。通过群体感应进行的细菌通讯已被证明可以通过生物膜基因的调节来影响生物膜的生长。我们的研究通过对群体信号的快速趋化反应揭示了群体感应在生物膜中的新作用。具体来说，我们研究了通用群体信号自诱导子 2 (AI-2) 对幽门螺杆菌的化学排斥如何塑造其生物膜的空间组织。我们证明，幽门螺杆菌对 AI-2 的化学脉冲反应对于促进其从非生物和生物表面生长的生物膜中的分散是必要的，并且足以促进以趋化性依赖性方式的分散。这项工作对于理解内源产生的微生物化合物塑造环境中微生物群落的组装和空间组织的机制具有广泛的意义。
The gastric pathogen Helicobacter pylori forms biofilms on abiotic and biotic surfaces. We have shown previously that H. pylori perceives the quorum signal autoinducer-2 (AI-2) as a chemorepellent. We report here that H. pylori chemorepulsion from endogenous AI-2 influences the proportions and spatial organization of cells within biofilms. Strains that fail to produce AI-2 (∆luxS strains) or are defective for chemotaxis (∆cheA strains) formed more spatially homogenous biofilms with a greater proportion of adherent versus planktonic cells than wild-type biofilms. Reciprocally, a strain that overproduced AI-2 (luxSOP) formed biofilms with proportionally fewer adherent cells. Along with the known AI-2 chemoreceptor, TlpB, we identified AibA and AibB, two novel periplasmic binding proteins that are required for the AI-2 chemorepulsion response. Disruptions in any of the proteins required for AI-2 chemotaxis recapitulated the biofilm adherence and spatial organization phenotype of the ∆luxS mutant. Furthermore, exogenous administration of AI-2 was sufficient to decrease the proportion of adherent cells in biofilms and promote dispersal of cells from biofilms in a chemotaxis-dependent manner. Finally, we found that disruption of AI-2 production or AI-2 chemotaxis resulted in increased clustering of cells in microcolonies on cultured epithelial cells. We conclude that chemotaxis from AI-2 is a determinant of H. pylori biofilm spatial organization and dispersal. Bacterial biofilms are ubiquitous in nature, but the mechanisms governing their assembly and spatial organization are not fully understood. Bacterial communication through quorum sensing has been shown to influence biofilm growth through the regulation of biofilm genes. Our study revealed a new role for quorum sensing in biofilms through rapid chemotactic responses to quorum signals. Specifically, we studied how chemorepulsion of Helicobacter pylori from the universal quorum signal autoinducer-2 (AI-2) shapes the spatial organization of its biofilms. We demonstrate that the chemorepulsive response of H. pylori to AI-2 is necessary to promote its dispersal from biofilms grown on both abiotic and biotic surfaces and is sufficient to promote dispersal in a chemotaxis-dependent manner. This work has broad implications for understanding the mechanisms by which endogenously produced microbial compounds shape the assembly and spatial organization of microbial communities in their environments.