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首页> 外文期刊>Infection and immunity >The CpAL Quorum Sensing System Regulates Production of Hemolysins CPA and PFO To Build Clostridium perfringens Biofilms
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The CpAL Quorum Sensing System Regulates Production of Hemolysins CPA and PFO To Build Clostridium perfringens Biofilms

机译：CpAL法定人数感应系统调节溶血素CPA和PFO的生产，以构建产气荚膜梭菌生物膜

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Clostridium perfringens strains produce severe diseases, including myonecrosis and enteritis necroticans, in humans and animals. Diseases are mediated by the production of potent toxins that often damage the site of infection, e.g., skin epithelium during myonecrosis. In planktonic cultures, the regulation of important toxins, such as CPA, CPB, and PFO, is controlled by the C. perfringens Agr-like (CpAL) quorum sensing (QS) system. Strains also encode a functional LuxS/AI-2 system. Although C. perfringens strains form biofilm-like structures, the regulation of biofilm formation is poorly understood. Therefore, our studies investigated the role of CpAL and LuxS/AI-2 QS systems and of QS-regulated factors in controlling the formation of biofilms. We first demonstrate that biofilm production by reference strains differs depending on the culture medium. Increased biomass correlated with the presence of extracellular DNA in the supernatant, which was released by lysis of a fraction of the biofilm population and planktonic cells. Whereas ΔagrB mutant strains were not able to produce biofilms, a ΔluxS mutant produced wild-type levels. The transcript levels of CpAL-regulated cpa and pfoA genes, but not cpb, were upregulated in biofilms compared to planktonic cultures. Accordingly, Δcpa and ΔpfoA mutants, in type A (S13) or type C (CN3685) backgrounds, were unable to produce biofilms, whereas CN3685Δcpb made wild-type levels. Biofilm formation was restored in complemented Δcpa/cpa and ΔpfoA/pfoA strains. Confocal microscopy studies further detected CPA partially colocalizing with eDNA on the biofilm structure. Thus, CpAL regulates biofilm formation in C. perfringens by increasing levels of certain toxins required to build biofilms.
机译：产气荚膜梭菌菌株在人和动物中产生严重的疾病，包括肌坏死和坏死性肠炎。疾病是由强效毒素的产生介导的，强效毒素通常会损害感染部位，例如在坏死性骨髓炎期间皮肤上皮。在浮游文化中，重要毒素（例如CPA，CPB和PFO）的调节由产气荚膜梭菌Agr样（CpAL）群体感应（QS）系统控制。菌株还编码功能性的LuxS / AI-2系统。尽管产气荚膜梭菌菌株形成生物膜样结构，但对生物膜形成的调控了解甚少。因此，我们的研究调查了CpAL和LuxS / AI-2 QS系统以及QS调节因子在控制生物膜形成中的作用。我们首先证明参考菌株的生物膜生产取决于培养基。生物量的增加与上清液中细胞外DNA的存在有关，上清液是通过一部分生物膜种群和浮游细胞的裂解而释放的。 ΔagrB突变株无法产生生物膜，而ΔluxS突变株则产生野生型水平。与浮游培养相比，生物膜中CpAL调节的cpa和pfoA基因而不是cpb的转录水平上调。因此，在A型（S13）或C型（CN3685）背景下的Δcpa和ΔpfoA突变体无法产生生物膜，而CN3685Δcpb则达到了野生型水平。在互补的Δcpa/ cpa和ΔpfoA/ pfoA菌株中，生物膜形成得以恢复。共聚焦显微镜研究进一步检测到CPA与eDNA在生物膜结构上部分共定位。因此，CpAL通过增加构建生物膜所需的某些毒素的水平来调节产气荚膜梭菌中生物膜的形成。

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