Service of Infectious Diseases, University Hospital Geneva and Department of Microbiology and Molecular Medicine, University of Geneva, Geneva, Switzerland.
PLoS Pathog. 2010 May 6;6(5):e1000883. doi: 10.1371/journal.ppat.1000883.
With the rising development of bacterial resistance the search for new medical treatments beyond conventional antimicrobials has become a key aim of public health research. Possible innovative strategies include the inhibition of bacterial virulence. However, consideration must be given to the evolutionary and environmental consequences of such new interventions. Virulence and cooperative social behaviour of the bacterium Pseudomonas aeruginosa rely on the quorum-sensing (QS) controlled production of extracellular products (public goods). Hence QS is an attractive target for anti-virulence interventions. During colonization, non-cooperating (and hence less virulent) P. aeruginosa QS-mutants, benefiting from public goods provided by wild type isolates, naturally increase in frequency providing a relative protection from invasive infection. We hypothesized that inhibition of QS-mediated gene expression removes this growth advantage and selection of less virulent QS-mutants, and maintains the predominance of more virulent QS-wild type bacteria. We addressed this possibility in a placebo-controlled trial investigating the anti-QS properties of azithromycin, a macrolide antibiotic devoid of bactericidal activity on P. aeruginosa, but interfering with QS, in intubated patients colonized by P. aeruginosa. In the absence of azithromycin, non-cooperating (and hence less virulent) lasR (QS)-mutants increased in frequency over time. Azithromycin significantly reduced QS-gene expression measured directly in tracheal aspirates. Concomitantly the advantage of lasR-mutants was lost and virulent wild-type isolates predominated during azithromycin treatment. We confirmed these results in vitro with fitness and invasion experiments. Azithromycin reduced growth rate of the wild-type, but not of the lasR-mutant. Furthermore, the lasR-mutant efficiently invaded wild-type populations in the absence, but not in the presence of azithromycin. These in vivo and in vitro results demonstrate that anti-virulence interventions based on QS-blockade diminish natural selection towards reduced virulence and therefore may increase the prevalence of more virulent genotypes in the Hospital environment. More generally, the impact of intervention on the evolution of virulence of pathogenic bacteria should be assessed.
随着细菌耐药性的不断上升,寻找超越传统抗菌药物的新医疗方法已成为公共卫生研究的主要目标。可能的创新策略包括抑制细菌的毒力。然而,必须考虑到这些新干预措施的进化和环境后果。铜绿假单胞菌的毒力和合作社会行为依赖于群体感应(QS)控制的细胞外产物(公共物品)的产生。因此,QS 是抗毒力干预的一个有吸引力的目标。在定植过程中,非合作(因此毒力较低)的铜绿假单胞菌 QS 突变体从野生型分离株提供的公共物品中受益,自然增加频率,从而提供相对的侵袭性感染保护。我们假设抑制 QS 介导的基因表达会消除这种生长优势,并选择毒力较低的 QS 突变体,从而维持毒力较高的 QS 野生型细菌的优势。我们在一项安慰剂对照试验中研究了阿奇霉素的抗 QS 特性,阿奇霉素是一种缺乏对铜绿假单胞菌杀菌活性的大环内酯类抗生素,但能干扰 QS,试验对象为被铜绿假单胞菌定植的插管患者。在没有阿奇霉素的情况下,非合作(因此毒力较低)的 lasR(QS)突变体随着时间的推移频率增加。阿奇霉素显著降低了直接从气管抽吸物中测量的 QS 基因表达。同时,lasR 突变体的优势丧失,在阿奇霉素治疗期间,毒力较强的野生型分离株占优势。我们在体外通过适应性和侵袭性实验证实了这些结果。阿奇霉素降低了野生型的生长速度,但 lasR 突变体没有。此外,lasR 突变体在没有阿奇霉素的情况下有效地侵入了野生型种群,但在有阿奇霉素的情况下没有。这些体内和体外的结果表明,基于 QS 阻断的抗毒力干预减少了对低毒力的自然选择,因此可能会增加医院环境中更毒力基因型的流行。更广泛地说,应该评估干预措施对致病菌毒力进化的影响。