Smith Brooke L, Zhang Meiyi, King Maria D
Aerosol Technology Laboratory, Biological and Agricultural Engineering Department, Texas A&M University, College Station, TX, 77843, USA.
Sci Rep. 2025 Jan 17;15(1):2349. doi: 10.1038/s41598-025-86562-2.
Gram-negative bacteria pose an increased threat to public health because of their ability to evade the effects of many antimicrobials with growing antibiotic resistance globally. One key component of gram-negative bacteria resistance is the functionality and the cells' ability to repair the outer membrane (OM) which acts as a barrier for the cell to the external environment. The biosynthesis of lipids, particularly lipopolysaccharides, or lipooligosaccharides (LPS/LOS) is essential for OM repair. Here we show the phenotypic and genotypic changes of Escherichia coli MG1655 (E. coli) before and after exposure to short-term aerosolization, 5 min, and long-term indoor aerosolization, 30 min. Short-term aerosolization samples exhibited major damages to the OM and resulted in the elongation of the cells. Long-term aerosolization seemed to lead to cell lysis and aggregation of cell material. Disintegrated OM rendered some of the elongated cells susceptible to cytoplasmic leakage and other damages. Further analysis of the repairs the E. coli cells seemed to enact after short-term aerosolization revealed that the repair molecules were likely lipid-containing droplets that perfectly countered the air pressure impacting the E. coli cells. If lipid biosynthesis to counter the pressure is inhibited in bacteria that are exposed to environmental conditions with high air velocity, the cells would lyse or be exposed to more toxins and thus become more susceptible to antimicrobial treatments. This article is the first to show lipid behavior in response to aerosolization stress in airborne bacteria both genotypically and phenotypically. Understanding the relationship between environmental conditions in ventilated spaces, lipid biosynthesis, and cellular responses is crucial for developing effective strategies to combat bacterial infections and antibiotic resistance. By elucidating the repair mechanisms initiated by E. coli in response to aerosolization, this study contributes to the broader understanding of bacterial adaptation and vulnerability under specific environmental pressures. These insights may pave the way for novel therapeutic approaches that target lipid biosynthesis pathways and exploit vulnerabilities in bacterial defenses, ultimately improving treatment outcomes.
革兰氏阴性菌对公众健康构成了越来越大的威胁，因为它们能够逃避许多抗菌药物的作用，且全球范围内抗生素耐药性不断增强。革兰氏阴性菌耐药性的一个关键组成部分是外膜（OM）的功能以及细胞修复外膜的能力，外膜是细胞与外部环境之间的屏障。脂质的生物合成，特别是脂多糖或脂寡糖（LPS/LOS）对于外膜修复至关重要。在这里，我们展示了大肠杆菌MG1655（E. coli）在短期雾化（5分钟）和长期室内雾化（30分钟）前后的表型和基因型变化。短期雾化样本显示外膜受到严重损伤，并导致细胞伸长。长期雾化似乎导致细胞裂解和细胞物质聚集。解体的外膜使一些伸长的细胞容易发生细胞质泄漏和其他损伤。对大肠杆菌细胞在短期雾化后似乎进行的修复的进一步分析表明，修复分子可能是含脂液滴，它们完美地抵消了影响大肠杆菌细胞的气压。如果在暴露于高风速环境条件下的细菌中，抑制用于抵抗压力的脂质生物合成，细胞将裂解或暴露于更多毒素，从而更容易受到抗菌治疗的影响。本文首次从基因型和表型上展示了空气传播细菌中脂质对雾化应激的反应行为。了解通风空间中的环境条件、脂质生物合成和细胞反应之间的关系对于制定有效的策略来对抗细菌感染和抗生素耐药性至关重要。通过阐明大肠杆菌对雾化的反应所启动的修复机制，本研究有助于更广泛地理解细菌在特定环境压力下的适应性和脆弱性。这些见解可能为针对脂质生物合成途径并利用细菌防御中的脆弱性的新型治疗方法铺平道路，最终改善治疗效果。
