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<p>The colonization and persistence of <i>Pseudomonas aeruginosa</i> in chronically diseased lungs are driven by various virulence factors. However, pulmonary infections in cystic fibrosis (CF) patients are predominantly polymicrobial. While <i>Achromobacter xylosoxidans</i> is an opportunistic pathogen in these patients, its impact on <i>P. aeruginosa</i> virulence during co-infection remains largely unknown. This study investigated <i>P. aeruginosa</i> interaction with two clonally related <i>A. xylosoxidans</i> strains, Ax 198 and Ax 200, co-isolated from CF sputum. We found that the interaction was strain-dependent, with Ax 200 significantly reducing <i>P. aeruginosa</i> virulence in a zebrafish model, providing the first <i>in vivo</i> evidence of this interaction. Proteomic analysis revealed that <i>P. aeruginosa</i> proteome was differently impacted by the two <i>A. xylosoxidans</i> strains, with Ax 200 altering proteins involved in biofilm formation, swimming motility, iron acquisition, and secretion systems. These findings were validated by phenotypic assays, confirming that <i>A. xylosoxidans</i> affected major <i>P. aeruginosa</i> virulence phenotypes, including biofilm formation, swimming motility, and siderophore production. Genetic analysis confirmed that distinct regulatory mechanisms, including iron cycle pathways, may account for the strain-dependent effects. These findings reveal a novel multi-target competitive mechanism through which <i>A. xylosoxidans</i> significantly disrupts <i>P. aeruginosa</i> virulence.</p>

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Achromobacter xylosoxidans modulates Pseudomonas aeruginosa virulence through a complex multi-target competition

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年7月2日

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  • Alison Besse,
  • Quentin Menetrey,
  • Vincent Jean-Pierre,
  • Sylvaine Huc-Brandt,
  • Fabien Aujoulat,
  • Chloé Dupont,
  • Raphaël Chiron,
  • Jean Armengaud,
  • Estelle Jumas-Bilak,
  • Virginie Molle,
  • Lucia Grenga,
  • Hélène Marchandin

摘要

The colonization and persistence of Pseudomonas aeruginosa in chronically diseased lungs are driven by various virulence factors. However, pulmonary infections in cystic fibrosis (CF) patients are predominantly polymicrobial. While Achromobacter xylosoxidans is an opportunistic pathogen in these patients, its impact on P. aeruginosa virulence during co-infection remains largely unknown. This study investigated P. aeruginosa interaction with two clonally related A. xylosoxidans strains, Ax 198 and Ax 200, co-isolated from CF sputum. We found that the interaction was strain-dependent, with Ax 200 significantly reducing P. aeruginosa virulence in a zebrafish model, providing the first in vivo evidence of this interaction. Proteomic analysis revealed that P. aeruginosa proteome was differently impacted by the two A. xylosoxidans strains, with Ax 200 altering proteins involved in biofilm formation, swimming motility, iron acquisition, and secretion systems. These findings were validated by phenotypic assays, confirming that A. xylosoxidans affected major P. aeruginosa virulence phenotypes, including biofilm formation, swimming motility, and siderophore production. Genetic analysis confirmed that distinct regulatory mechanisms, including iron cycle pathways, may account for the strain-dependent effects. These findings reveal a novel multi-target competitive mechanism through which A. xylosoxidans significantly disrupts P. aeruginosa virulence.