高铁酸盐(Fe(VI))是一种环保消毒剂,广泛用于根除再生水中的微生物。然而,吸入经Fe(VI)处理的含细菌再生水的潜在健康风险仍不确定.我们旨在探讨K2FeO4处理的大肠杆菌(E.大肠杆菌ATCC25922)。我们的发现表明,Fe(VI)消毒诱导了剂量和时间依赖性的大肠杆菌灭活,伴随着细菌内毒素的快速释放,脂多糖(LPS)。扫描电子显微镜(SEM)观察表明,Fe(VI)诱导的内毒素产生至少包括两个阶段:内毒素与细菌的初始结合以及随后的解离以释放游离内毒素。此外,Fe(VI)消毒不能有效地消除纯的或大肠杆菌衍生的内毒素。本研究中使用的大肠杆菌菌株缺乏肺部感染能力,因此,单独吸入细菌不会引起严重的肺损伤。然而,小鼠吸入暴露于Fe(VI)处理的大肠杆菌显示肺结构和功能的严重损害。此外,我们观察到中性粒细胞/巨噬细胞募集的积累,细胞凋亡,和在经受Fe(VI)处理的大肠杆菌的小鼠的肺组织中的ROS产生。RNA测序(RNA-seq)和PCR结果显示,与内毒素刺激有关的基因,细胞凋亡,抗氧化防御,炎症反应,趋化因子及其受体响应于Fe(VI)处理的大肠杆菌而上调。总之,Fe(VI)在消除内毒素方面是无效的,并且由于从灭活的细菌释放内毒素而可引发继发性危害。气溶胶暴露于Fe(VI)处理的大肠杆菌通过诱导氧化应激和炎症反应对肺组织造成相当大的损害。
Ferrate (Fe(VI)) is an environmentally friendly disinfectant that is widely used to eradicate microbes in reclaimed water. However, the potential health risks associated with inhalation of Fe(VI)-treated bacteria-laden reclaimed water remains uncertain. We aimed to explore the inhalation hazards and potential mechanisms of K2FeO4-treated Escherichia coli (E. coli, ATCC 25922). Our findings indicated that Fe(VI) disinfection induced a dose- and time-dependent E. coli inactivation, accompanied by a rapid release of the bacterial endotoxin, lipopolysaccharide (LPS). Scanning electron microscopy (SEM) observations indicate that Fe(VI)-induced endotoxin production consists of at least two stages: initial binding of endotoxin to bacteria and subsequent dissociation to release free endotoxin. Furthermore, Fe(VI) disinfection was not able to effectively eliminate pure or E. coli-derived endotoxins. The E. coli strain used in this study lacks lung infection capability, thus the inhalation of bacteria alone failed to induce severe lung injury. However, mice inhaled exposure to Fe(VI)-treated E. coli showed severe impairment of lung structure and function. Moreover, we observed an accumulation of neutrophil/macrophage recruitment, cell apoptosis, and ROS generation in the lung tissue of mice subjected to Fe(VI)-treated E. coli. RNA sequencing (RNA-seq) and PCR results revealed that genes involved with endotoxin stimuli, cell apoptosis, antioxidant defence, inflammation response, chemokines and their receptors were upregulated in response to Fe(VI)-treated E. coli. In conclusion, Fe(VI) is ineffective in eliminating endotoxins and can trigger secondary hazards owing to endotoxin release from inactivated bacteria. Aerosol exposure to Fe(VI)-treated E. coli causes considerable damage to lung tissue by inducing oxidative stress and inflammatory responses.