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Peer-reviewedCC BY 4.0Molecules

Isoliquiritigenin Modulates Quorum Sensing-Associated Neutrophil Extracellular Trap Formation in COPD Isolate Pseudomonas aeruginosa

  • Honagodu Ravichandra Dhanyashree1
  • Rakshitha Charavu2
  • Asif Hameed1,3,4
  • Kizhakkumkara Karthika1
  • Adarsh Basavaraj Mynalli5
  • Suprith Surya6
  • Yashodhar Prabhakar Bhandary2
  • Rajesh Padumane Shastry1,3,4
6 affiliations
  1. 1Division of Microbiology and Biotechnology, Yenepoya Research Centre, Yenepoya (Deemed to Be University), Deralakatte, Mangalore 575018, India
  2. 2Division of Cell Biology and Molecular Genetics, Yenepoya Research Centre, Yenepoya (Deemed to Be University), Deralakatte, Mangalore 575018, India
  3. 3Anaerobic & Translational Genomics Centre (ATGC), Yenepoya Research Centre, Yenepoya (Deemed to Be University), Deralakatte, Mangalore 575018, India
  4. 4Caenorhabditis elegans Laboratory Facility (CeLF), Yenepoya Research Centre, Yenepoya (Deemed to Be University), Deralakatte, Mangalore 575018, India
  5. 5Department of Respiratory Medicine, Yenepoya Medical College Hospital, Deralakatte, Mangalore 575018, India
  6. 6Advanced Surgical Skill ENhancement Division (ASSEND), Yenepoya (Deemed to Be University), Deralakatte, Mangalore 575018, India
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Abstract

We characterize a virulent COPD isolate, P. aeruginosa RS85, as a potential inducer of NET, and demonstrate the ameliorating impacts of isoliquiritigenin (ISL) on bacterial quorum sensing (QS) and neutrophil responses. Low doses of ISL exhibited anti-quorum sensing (AQS) activities on P. aeruginosa RS85 and PAO1, while its high dose was found to be bactericidal. Significantly high amounts of ROS and NETosis were observed in neutrophils when treated with the live cells and secretome of clinical P. aeruginosa, whereas P. aeruginosa PAO1-JP2 elicited markedly reduced responses. RS85 secretome promoted pulmonary NET formation, recruitment of inflammatory cells, alveolar destruction, and emphysema-like pathology in mouse lungs in vivo. The introduction of ISL inhibited cell- and secretome-mediated ROS and NETosis to the levels observed in PAO1-JP2. ISL treatment constrained NETosis, the co-localization of myeloperoxidase and citrullinated histone H3, lung inflammatory damage and structural damage in vivo. The molecular docking of ISL with bacterial QS (LasR and RhlR) and neutrophil NADPH oxidase assembly (p47phox and NOX2) proteins showed strong ligand binding, substantiating interference in QS signaling and ROS generation pathways. This study identifies potential QS-regulated secretory virulence in clinical P. aeruginosa driving NETosis, and demonstrates the ISL-mediated amelioration of NETs and bacterial QS.

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Cite

BibTeXRIS
BibTeX
@article{dhanyashree2026isoliquiritigenin,
  title = {{Isoliquiritigenin Modulates Quorum Sensing-Associated Neutrophil Extracellular Trap Formation in COPD Isolate Pseudomonas aeruginosa}},
  author = {Honagodu Ravichandra Dhanyashree and Rakshitha Charavu and Asif Hameed and Kizhakkumkara Karthika and Adarsh Basavaraj Mynalli and Suprith Surya and Yashodhar Prabhakar Bhandary and Rajesh Padumane Shastry},
  journal = {Molecules},
  year = {2026},
  month = nov,
  doi = {10.3390/molecules31214007},
  url = {https://www.mdpi.com/1420-3049/31/21/4007},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Isoliquiritigenin Modulates Quorum Sensing-Associated Neutrophil Extracellular Trap Formation in COPD Isolate Pseudomonas aeruginosa
AU  - Honagodu Ravichandra Dhanyashree
AU  - Rakshitha Charavu
AU  - Asif Hameed
AU  - Kizhakkumkara Karthika
AU  - Adarsh Basavaraj Mynalli
AU  - Suprith Surya
AU  - Yashodhar Prabhakar Bhandary
AU  - Rajesh Padumane Shastry
PY  - 2026
DA  - 2026/11/06
JO  - Molecules
DO  - 10.3390/molecules31214007
UR  - https://www.mdpi.com/1420-3049/31/21/4007
AB  - We characterize a virulent COPD isolate, P. aeruginosa RS85, as a potential inducer of NET, and demonstrate the ameliorating impacts of isoliquiritigenin (ISL) on bacterial quorum sensing (QS) and neutrophil responses. Low doses of ISL exhibited anti-quorum sensing (AQS) activities on P. aeruginosa RS85 and PAO1, while its high dose was found to be bactericidal. Significantly high amounts of ROS and NETosis were observed in neutrophils when treated with the live cells and secretome of clinical P. aeruginosa, whereas P. aeruginosa PAO1-JP2 elicited markedly reduced responses. RS85 secretome promoted pulmonary NET formation, recruitment of inflammatory cells, alveolar destruction, and emphysema-like pathology in mouse lungs in vivo. The introduction of ISL inhibited cell- and secretome-mediated ROS and NETosis to the levels observed in PAO1-JP2. ISL treatment constrained NETosis, the co-localization of myeloperoxidase and citrullinated histone H3, lung inflammatory damage and structural damage in vivo. The molecular docking of ISL with bacterial QS (LasR and RhlR) and neutrophil NADPH oxidase assembly (p47phox and NOX2) proteins showed strong ligand binding, substantiating interference in QS signaling and ROS generation pathways. This study identifies potential QS-regulated secretory virulence in clinical P. aeruginosa driving NETosis, and demonstrates the ISL-mediated amelioration of NETs and bacterial QS.
SN  - 1420-3049
ER  -