Harnessing CRISPR interference to re-sensitize laboratory strains and clinical isolates to last resort antibiotics

Angelica Frusteri Chiacchiera, Michela Casanova, Massimo Bellato, Aurora Piazza, Roberta Migliavacca, Gregory Batt, Paolo Magni, Lorenzo Pasotti
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Abstract

The global race against antimicrobial resistance requires novel antimicrobials that are not only effective in killing specific bacteria, but also minimize the emergence of new resistances. Recently, CRISPR/Cas-based antimicrobials were proposed to address killing specificity with encouraging results. However, the emergence of target sequence mutations triggered by Cas-cleavage was identified as an escape strategy, posing the risk of generating new antibiotic-resistance gene (ARG) variants. Here, we evaluated an antibiotic re-sensitization strategy based on CRISPR interference (CRISPRi), which inhibits gene expression without damaging target DNA. The resistance to four antibiotics, including last resort drugs, was significantly reduced by individual and multi-gene targeting of ARGs in low- to high-copy numbers in recombinant E. coli. Escaper analysis confirmed the absence of mutations in target sequence, corroborating the harmless role of CRISPRi in the selection of new resistances. E. coli clinical isolates carrying ARGs of severe clinical concern were then used to test the robustness of CRISPRi under different growth conditions. Meropenem, colistin and cefotaxime susceptibility was successfully increased in terms of MIC (up to >4-fold) and growth delay (up to 11-hours) in a medium-dependent fashion. To our knowledge, this is the first demonstration of CRISPRi-mediated re-sensitization to last-resort drugs in clinical isolates. This study laid the foundations for further leveraging CRISPRi as antimicrobial agent or research tool to selectively repress ARGs and investigate resistance mechanisms.
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利用 CRISPR 干扰使实验室菌株和临床分离菌株对最后的抗生素重新敏感
全球对抗抗菌药耐药性的竞赛要求新型抗菌药不仅能有效杀死特定细菌,还能最大限度地减少新耐药性的出现。最近,人们提出了基于 CRISPR/Cas 的抗菌药物来解决杀灭特异性问题,并取得了令人鼓舞的成果。然而,Cas清除引发的靶序列突变被认为是一种逃逸策略,有可能产生新的抗生素耐药基因(ARG)变体。在这里,我们评估了一种基于CRISPR干扰(CRISPRi)的抗生素再敏感化策略,它能抑制基因表达而不损伤靶DNA。在重组大肠杆菌中,通过对低拷贝数到高拷贝数的 ARGs 进行单基因和多基因靶向,对四种抗生素(包括最后一种药物)的耐药性显著降低。Escaper分析证实了靶序列中没有突变,证实了CRISPRi在新抗药性选择中的无害作用。然后,使用携带严重临床问题 ARGs 的大肠杆菌临床分离株来测试 CRISPRi 在不同生长条件下的稳健性。美罗培南、秋水仙碱和头孢他啶的敏感性成功地在 MIC(高达 4 倍)和生长延迟(长达 11 小时)方面得到了提高,而生长延迟则取决于培养基。据我们所知,这是首次证明 CRISPRi- 介导的临床分离物对最后一种药物的再敏感性。这项研究为进一步利用 CRISPRi 作为抗菌剂或研究工具来选择性抑制 ARGs 和研究抗药性机制奠定了基础。
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