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N-acetyl-glucosamine primes Pseudomonas aeruginosa for virulence through a type IV pili/cAMP-mediated morphology

Jing Chen1, Guiying Lin2,3,4, Kaiyu Ma2

  • 1Sino-French Hoffmann Institute, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, China. chenjing_1127@qq.com.

Nature Communications
|October 24, 2025
PubMed

Insights

Pseudomonas aeruginosa requires a priming step for virulence, involving a shape change and resistance to antimicrobial peptides. This process is regulated by type IV pili effectors and sugar signaling molecules like N-acetylglucosamine (NAG).

Area of Science:

  • Microbiology
  • Pathogenesis
  • Bacterial Virulence

Background:

  • Pathogenic microbes must survive host defenses and proliferate to cause infection.
  • The mechanisms by which bacteria resist immune responses and transition to virulence are not fully understood.
  • Pseudomonas aeruginosa is an opportunistic pathogen relevant to studying virulence.

Purpose of the Study:

  • To investigate the maturation step, termed priming, required for Pseudomonas aeruginosa virulence in a Drosophila infection model.
  • To elucidate the molecular mechanisms underlying bacterial priming and resistance to host defenses.

Main Methods:

  • Utilized a Drosophila melanogaster model for acute bacterial infection.
  • Investigated the role of type IV pili (T4P) effectors (FimV, Vfr) and peptidoglycan synthesis in bacterial priming.
  • Examined the impact of N-acetyl-muramic acid (NAM) and N-acetylglucosamine (NAG) on bacterial morphology, virulence, and T4P localization.

Main Results:

  • Planktonic Pseudomonas aeruginosa requires a priming step for virulence, involving a switch to bacillus shape and resistance to antimicrobial peptides in vivo.
  • Priming necessitates an interplay between T4P effectors FimV and Vfr, enhancing lateral cell wall peptidoglycan synthesis.
  • N-acetyl-muramic acid (NAM) inhibits virulence by inducing a round shape and disrupting FimV polar localization and cAMP signaling.
  • N-acetylglucosamine (NAG) promotes FimV polar placement, counteracts NAM, and accelerates priming in a PilJ-dependent manner.

Conclusions:

  • Bacterial priming is a critical maturation step for Pseudomonas aeruginosa virulence, involving morphological changes and immune evasion.
  • Type IV pili components FimV and Vfr, along with peptidoglycan synthesis, are key regulators of this priming process.
  • N-acetylglucosamine (NAG) acts as a signaling molecule that promotes bacterial virulence through morphological switching, a mechanism potentially conserved across different microbial pathogens.

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