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<p><i>Cystic fibrosis</i> (CF) is a genetic lung disease in which thick mucus builds up in the airways, making patients highly vulnerable to chronic bacterial infections. One of the most problematic bacteria in these infections is <i>Pseudomonas aeruginosa</i>, an adaptable microbe that can survive antibiotics and persist in the lungs for many years. This bacterium uses a communication system called “quorum sensing (QS)” to coordinate group behaviors. Through this system, bacterial cells sense their population density and collectively switch on genes that control toxin production, biofilm formation, and resistance to treatment. In cystic fibrosis lungs, the protective lung surfactant layer, especially a major lipid component called dipalmitoylphosphatidylcholine (DPPC), becomes altered due to chronic inflammation. Emerging evidence suggests that altered surfactant lipids may influence bacterial behavior in addition to reflecting lung damage. Instead, they may actively signal to <i>P. aeruginosa</i>, triggering its QS system earlier than expected. This early activation promotes virulence, biofilm persistence, and long-term infection. This review highlights how host lung lipids interact with bacterial communication networks and discuss how targeting QS using surfactant-inspired molecules may offer new therapeutic strategies. Understanding this host–pathogen interaction could lead to innovative anti virulence treatments that weaken the bacteria without directly killing them, potentially reducing antibiotic resistance.</p>

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Surfactant-driven quorum sensing of Pseudomonas aeruginosa in cystic fibrosis

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年6月16日

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  • Prathibha Selvamani,
  • James John,
  • Janaki Devi Kumar,
  • Sangeetha Gopalakrishnan,
  • Jagadish Chandra Kumar Mangu,
  • Priyatharshini Thangaraj,
  • Krupakar parthasarathy

摘要

Cystic fibrosis (CF) is a genetic lung disease in which thick mucus builds up in the airways, making patients highly vulnerable to chronic bacterial infections. One of the most problematic bacteria in these infections is Pseudomonas aeruginosa, an adaptable microbe that can survive antibiotics and persist in the lungs for many years. This bacterium uses a communication system called “quorum sensing (QS)” to coordinate group behaviors. Through this system, bacterial cells sense their population density and collectively switch on genes that control toxin production, biofilm formation, and resistance to treatment. In cystic fibrosis lungs, the protective lung surfactant layer, especially a major lipid component called dipalmitoylphosphatidylcholine (DPPC), becomes altered due to chronic inflammation. Emerging evidence suggests that altered surfactant lipids may influence bacterial behavior in addition to reflecting lung damage. Instead, they may actively signal to P. aeruginosa, triggering its QS system earlier than expected. This early activation promotes virulence, biofilm persistence, and long-term infection. This review highlights how host lung lipids interact with bacterial communication networks and discuss how targeting QS using surfactant-inspired molecules may offer new therapeutic strategies. Understanding this host–pathogen interaction could lead to innovative anti virulence treatments that weaken the bacteria without directly killing them, potentially reducing antibiotic resistance.