AI 中文总结
该研究发现β-内酰胺类抗生素诱导的细菌伸长会抑制趋流性，而抗性细菌因保持短形态保留趋流能力，据此可实现抗性细菌的微流控富集，为快速AMR检测提供了策略。
AI 中文摘要
抗菌耐药性（AMR）使肺部和尿路感染（UTIs）等疾病的治疗复杂化，这些是全球最常见的细菌感染。能动病原体可利用趋流性逆着液流上游游动，可能促进其进入解剖 tract 的上部区域。然而，抗生素暴露和耐药性如何影响这一转运过程仍不清楚。本研究利用单细胞追踪显微镜，探究β-内酰胺类抗生素诱导的伸长如何影响大肠杆菌在受限微流控通道中的趋流迁移。研究发现，即使易感的伸长细胞仍完全能动，抗生素仍可使趋流性抑制100倍；而在相同条件下，抗性细菌保持短形态并保留上游迁移能力。利用具有可调细胞长度的基因工程细菌，研究人员证实趋流性的潜在机制是细胞形态与流涡度的耦合，伸长细胞会被快速旋转至下游。最后，研究人员利用这种长度依赖的转运差异，在液流下分离短细胞与伸长细胞，并从混合群体中富集氨苄西林抗性细胞。综上，这些结果确立细菌伸长是趋流转运的关键控制参数，并为富集β-内酰胺类抗生素抗性细菌提供了概念验证策略，有望用于快速AMR检测。
英文摘要
Antimicrobial resistance (AMR) complicates the treatment of diseases including lung and urinary tract infections (UTIs), which are among the most common bacterial infections worldwide. Motile pathogens can use rheotaxis to swim upstream against fluid flows, potentially promoting access to upper regions of anatomical tracts. However, it remains unclear how antibiotic exposure and resistance influence this transport process. Here, using single-cell tracking microscopy, we investigate how elongation induced by \b{eta}-lactam antibiotics affects the rheotactic migration of E. coli in confined microfluidic channels. Remarkably, we find that rheotaxis can be inhibited 100-fold by antibiotics, even if the susceptible elongated cells remain fully motile. However, resistant bacteria remain short and retain upstream migration under the same conditions. Using genetically engineered bacteria with tunable cell length, we show that the underlying mechanism that governs rheotaxis is the coupling between cell morphology and flow vorticity, where elongated cells are rapidly rotated downstream. Finally, we exploit this length-dependent transport difference to separate short and elongated cells under flow and enrich ampicillin-resistant cells from mixed populations. Together, these results establish bacterial elongation as a key control parameter for rheotactic transport, and provide a proof-of-concept strategy for enriching \b{eta}-lactam-resistant bacteria for potential use in rapid AMR detection.
