目的:研究灵菌红素对肺炎克雷伯菌生物膜的影响及其机制,以期为临床治疗肺炎克雷伯菌提供新的治疗思路。方法:选择肺炎克雷伯菌NTUH-K2044菌株作为实验菌株,进行药敏实验、生长曲线测定、生物膜抑制实验以及RT-PCR实验,分析灵菌红素对肺炎克雷伯菌生长和生物膜的影响及相关机制。结果:灵菌红素对肺炎克雷伯菌的MIC值为256 μg/ml,灵菌红素对肺炎克雷伯菌的MBIC为64 μg/ml。灵菌红素在12 h内对肺炎克雷伯菌的I型菌毛基因(fimA, fimH, fimK)、III型菌毛基因(mrkD, mrkH)、荚膜多糖基因rmpA和毒力基因magA有抑制作用。灵菌红素在24 h时,对肺炎克雷伯菌生物膜的相关基因(除fimA,rmpA外)有负向调控作用。结论:灵菌红素能抑制肺炎克雷伯菌生长和生物膜形成,其可能的机制是下调肺炎克雷伯菌生物膜的相关基因(fimA, fimH, fimK, mrkD, mrkH, rmpA, magA)表达量。Objective: To investigate the effects of prodigiosin on the biofilm of Klebsiella pneumoniae and its mechanism, so as to provide a new therapeutic idea for the clinical treatment of Klebsiella pneumoniae. Methods: The NTUH-K2044 strain of Klebsiella pneumoniae was selected as the experimental strain. Antimicrobial susceptibility tests, growth curve determination, biofilm inhibition experiments, and RT-PCR experiments were performed to analyze the effects of prodigiosin on the growth and biofilm of Klebsiella pneumoniae and the related mechanisms. Results: The MIC value of prodigiosin against Klebsiella pneumoniae was 256 μg/ml, and the MBIC was 64 μg/ml. Prodigiosin had inhibitory effects on the type I fimbrial genes (fimA, fimH, fimK), type III fimbrial genes (mrkD, mrkH), capsular polysaccharide gene rmpA, and virulence gene magA of Klebsiella pneumoniae within 12 hours. At 24 hours, prodigiosin had negative regulatory effects on the biofilm-related genes of Klebsiella pneumoniae (except for fimA and rmpA). Conclusion: Prodigiosin can inhibit the growth and
