Université de Lorraine, CNRS, LIEC, Metz, France.
Université de Lorraine, CNRS, LIEC, Nancy, France.
Commun Biol. 2021 Jun 3;4(1):678. doi: 10.1038/s42003-021-02213-y.
Toxicity mechanisms of metal oxide nanoparticles towards bacteria and underlying roles of membrane composition are still debated. Herein, the response of lipopolysaccharide-truncated Escherichia coli K12 mutants to TiO nanoparticles (TiONPs, exposure in dark) is addressed at the molecular, single cell, and population levels by transcriptomics, fluorescence assays, cell nanomechanics and electrohydrodynamics. We show that outer core-free lipopolysaccharides featuring intact inner core increase cell sensitivity to TiONPs. TiONPs operate as membrane strippers, which induce osmotic stress, inactivate cell osmoregulation and initiate lipid peroxidation, which ultimately leads to genesis of membrane vesicles. In itself, truncation of lipopolysaccharide inner core triggers membrane permeabilization/depolarization, lipid peroxidation and hypervesiculation. In turn, it favors the regulation of TiONP-mediated changes in cell Turgor stress and leads to efficient vesicle-facilitated release of damaged membrane components. Remarkably, vesicles further act as electrostatic baits for TiONPs, thereby mitigating TiONPs toxicity. Altogether, we highlight antagonistic lipopolysaccharide-dependent bacterial responses to nanoparticles and we show that the destabilized membrane can generate unexpected resistance phenotype.
金属氧化物纳米颗粒对细菌的毒性机制以及膜成分的潜在作用仍存在争议。在此，通过转录组学、荧光分析、细胞纳米力学和电动流体动力学，在分子、单细胞和群体水平上研究了脂多糖截短的大肠杆菌 K12 突变体对 TiO 纳米颗粒（TiONPs，在黑暗中暴露）的反应。我们表明，具有完整核心的无外核脂多糖会增加细胞对 TiONPs 的敏感性。TiONPs 作为细胞膜剥离剂，会引发渗透胁迫，使细胞渗透压调节失活并引发脂质过氧化，最终导致膜泡的产生。脂多糖内核心的截短本身会引发细胞膜通透性/去极化、脂质过氧化和过度囊泡化。反过来，它有利于调节 TiONP 介导的细胞膨压变化，并导致受损膜成分的有效囊泡介导释放。值得注意的是，囊泡进一步充当 TiONPs 的静电诱饵，从而减轻 TiONPs 的毒性。总的来说，我们强调了细菌对纳米颗粒的拮抗脂多糖依赖性反应，并表明不稳定的细胞膜可以产生意想不到的耐药表型。
