PslG-Mediated Disruption of Pseudomonas aeruginosa Biofilms: A Multi-Omics Investigation of Matrix Glycan Release, Metabolic Reprogramming, and Structural Disintegration
- 1Beijing Research Institute of Traumatology and Orthopaedics, Beijing 100035, China
- 2Beijing Jishuitan Hospital, Capital Medical University, Beijing 100035, China
- 3State Key Laboratory of Microbial Diversity and Innovative Utilization, Institute of Microbiology, Chinese Academy of Sciences, Beijing 100101, China
Abstract
Pseudomonas aeruginosa biofilms are recalcitrant to conventional antibiotic therapy due to their extracellular polymeric substance (EPS) matrix, in which Psl polysaccharide serves as the primary structural scaffold. PslG glycoside hydrolase can degrade Psl and trigger biofilm dispersal, yet the dynamic glycan release profile and metabolic consequences remain poorly characterized. Mature P. aeruginosa PAO1 biofilms were treated with PslG (1–1000 nM) for 0–30 min. Biomass was quantified by crystal violet staining. Matrix glycan composition and untargeted metabolomics was performed using LC-MS/MS. Three-dimensional architecture was visualized by confocal laser scanning microscopy (CLSM) with SYTO 9/PI and HHA-FITC staining. PslG induced near-complete loss of Psl-specific fluorescence within 30 min. Counterintuitively, biofilm thickness decreased from 10.8 μm at baseline to approximately 3.0 μm at 5–10 min and partially recovered to 7.2 μm at 30 min, remaining below baseline; the recovery of thickness is progressively due to matrix swelling and bacterial vertical redistribution. PI staining revealed no membrane damage, confirming non-lethal dispersal. Glycomically, galactose, xylose and metabolic intermediates (glucose-6-phosphate) were enriched. Metabolomics revealed significant activation of pentose and glucuronate interconversions, pantothenate and CoA biosynthesis, carbon metabolism, and amino acid biosynthesis. The Psl cleavage mediated by PslG may trigger bacterial dispersal with vertical expansion and metabolic reprogramming toward a planktonic lifestyle. These findings provide mechanistic insights for designing Psl-targeted anti-biofilm therapeutics.
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BibTeX
@article{zheng2026pslgmediated,
title = {{PslG-Mediated Disruption of Pseudomonas aeruginosa Biofilms: A Multi-Omics Investigation of Matrix Glycan Release, Metabolic Reprogramming, and Structural Disintegration}},
author = {Yaqian Zheng and Zebin Gui and Yun Xue and You Zhou and Chaofeng Hu and Jingshuang Zhang and Luyan Z. Ma and Rui Shi},
journal = {International journal of molecular sciences},
year = {2026},
month = sep,
doi = {10.3390/ijms27198787},
url = {https://europepmc.org/article/PMC/PMC13664999},
note = {CC BY},
}
RIS
TY - JOUR
TI - PslG-Mediated Disruption of Pseudomonas aeruginosa Biofilms: A Multi-Omics Investigation of Matrix Glycan Release, Metabolic Reprogramming, and Structural Disintegration
AU - Yaqian Zheng
AU - Zebin Gui
AU - Yun Xue
AU - You Zhou
AU - Chaofeng Hu
AU - Jingshuang Zhang
AU - Luyan Z. Ma
AU - Rui Shi
PY - 2026
DA - 2026/09/30
JO - International journal of molecular sciences
DO - 10.3390/ijms27198787
UR - https://europepmc.org/article/PMC/PMC13664999
AB - Pseudomonas aeruginosa biofilms are recalcitrant to conventional antibiotic therapy due to their extracellular polymeric substance (EPS) matrix, in which Psl polysaccharide serves as the primary structural scaffold. PslG glycoside hydrolase can degrade Psl and trigger biofilm dispersal, yet the dynamic glycan release profile and metabolic consequences remain poorly characterized. Mature P. aeruginosa PAO1 biofilms were treated with PslG (1–1000 nM) for 0–30 min. Biomass was quantified by crystal violet staining. Matrix glycan composition and untargeted metabolomics was performed using LC-MS/MS. Three-dimensional architecture was visualized by confocal laser scanning microscopy (CLSM) with SYTO 9/PI and HHA-FITC staining. PslG induced near-complete loss of Psl-specific fluorescence within 30 min. Counterintuitively, biofilm thickness decreased from 10.8 μm at baseline to approximately 3.0 μm at 5–10 min and partially recovered to 7.2 μm at 30 min, remaining below baseline; the recovery of thickness is progressively due to matrix swelling and bacterial vertical redistribution. PI staining revealed no membrane damage, confirming non-lethal dispersal. Glycomically, galactose, xylose and metabolic intermediates (glucose-6-phosphate) were enriched. Metabolomics revealed significant activation of pentose and glucuronate interconversions, pantothenate and CoA biosynthesis, carbon metabolism, and amino acid biosynthesis. The Psl cleavage mediated by PslG may trigger bacterial dispersal with vertical expansion and metabolic reprogramming toward a planktonic lifestyle. These findings provide mechanistic insights for designing Psl-targeted anti-biofilm therapeutics.
SN - 1422-0067
ER -