基于基因聚类分析的大蒜素对耐碳青霉烯类肺炎克雷伯菌抑菌机制

Antibacterial mechanism of allicin against carbapenem-resistant Klebsiella pneumoniae based on gene cluster analysis

    摘要
  • 摘要:
    目的 研究大蒜素对耐碳青霉烯类肺炎克雷伯菌(CRKP)体外抑制作用机制。
    方法 采用标准微量肉汤稀释法, 确定大蒜素对实验使用CRKP的最低抑菌浓度(MIC)。绘制生长曲线, 验证大蒜素浓度与抑菌作用的关系。对大蒜素处理的CRKP和正常对照组进行转录组测序(RNA-seq), 探究大蒜素抑制CRKP生长的分子机制。
    结果 大蒜素对CRKP的MIC为140 mg/ml。筛选出正常对照组和大蒜素处理组共有1 775个差异基因, 其中845个基因表达上调, 930个基因表达下调, 细菌磷酸转移酶系统(PTS)基因表达在对照组和处理组中差异有统计学意义(P＜0.05), EIIA-EIID基因表达水平降低(P＜0.05)。
    结论 基于转录组测序结果分析发现, 大蒜素可能通过破坏CRKP的糖转运系统, 进而影响其生物膜形成, 以抑制其生长。

     

    Abstract:
    OBJECTIVE To investigate the in vitro inhibitory mechanism of allicin against carbapenem-resistant Klebsiella pneumoniae (CRKP).
    METHODS The standard microbroth dilution method was employed to determine the minimum inhibitory concentration (MIC) of allicin against the experimental CRKP. Growth curve experiments were conducted to verify the relationship between allicin concentration and antibacterial action. RNA sequencing (RNA-seq) was performed on allicin-treated CRKP and a normal control group to explore the molecular mechanism of allicin inhibiting CRKP growth.
    RESULTS The MIC of allicin against CRKP was 140 mg/ml. A total of 1 775 differentially expressed genes were screened from the normal control group and the allicin-treated group, with 845 genes upregulated and 930 genes downregulated. The expression of bacterial phosphotransferase system (PTS) genes showed significant differences between the control group and the treated group (P < 0.05), and the expression levels of EIIA-EIID genes decreased (P < 0.05).
    CONCLUSION Based on the analysis of RNA-seq results, it is found that allicin may inhibits the growth of CRKP by disrupting its sugar transport system, thereby affecting its biofilm formation.

     

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