Exploring the antibacterial potential of arthrocolins against extensively drug-resistant Pseudomonas aeruginosa: mechanistic insights into amino acid metabolism disruption

探索关节素类化合物对广泛耐药铜绿假单胞菌的抗菌潜力:氨基酸代谢紊乱的机制研究

阅读:1

Abstract

INTRODUCTION: Extensively drug-resistant Pseudomonas aeruginosa (XDR-PA) poses a serious clinical threat due to its intrinsic resistance mechanisms and the lack of effective therapeutic agents. This study aimed to evaluate the antibacterial activity of arthrocolins (Acs), a novel group of xanthene-like compounds isolated from Escherichia coli, against XDR-PA. METHODS: Clinical data analysis was conducted to identify significant risk factors for XDR-PA infection. Drug susceptibility testing was performed to assess the effectiveness of Acs. Transmission electron microscopy (TEM) was used to observe cellular changes in Acs-treated bacteria, while integrated transcriptomic and metabolomic analyses were employed to investigate the underlying mechanisms. RESULTS: Acs demonstrated significant antibacterial activity, inhibiting XDR-PA growth at low micromolar concentrations. The IC50 value was determined to be 3.094 μM. Clinical data analysis identified prolonged antimicrobial therapy, invasive procedures, and extended hospitalization as significant risk factors for XDR-PA infection. TEM revealed cell wall disruption and cytoplasmic condensation in Acs-treated bacteria. Integrated omics analyses indicated that Acs interferes with amino acid metabolism, impairing energy production and causing abnormal lipid accumulation. DISCUSSION: These findings suggest that Acs exerts potent antibacterial effects through disruption of metabolic homeostasis and structural integrity. The study highlights the potential of Acs as a promising candidate for the treatment of XDR-PA infections, offering a new avenue for therapeutic development. The bacterial names cannot be italicized in the annotations. The revised abstract has been uploaded separately as an attachment.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。