Wza gene knockout decreases Acinetobacter baumannii virulence and affects Wzy-dependent capsular polysaccharide

Tianshui Niu1,2, Lihua Guo1, Qixia Luo1

  • 1Collaborative Initiative Center for Diagnosis and Treatment of Infectious Diseases, State Key Laboratory for Diagnosis & Treatment of Infectious Diseases, the First Affiliated Hospital, college of Medicine, Zhejiang University, Hangzhou, China.

Virulence
|December 28, 2019
PubMed

Insights

The capsular polysaccharide export protein (Wza) in carbapenem-resistant Acinetobacter baumannii significantly impacts bacterial virulence. Knocking out the wza gene reduces virulence, affecting capsule formation and gene expression, with complementation restoring these traits.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Infectious Diseases

Background:

  • Carbapenem-resistant *Acinetobacter baumannii* (CRAB) poses a significant threat due to its multidrug resistance.
  • Capsular polysaccharides play a crucial role in bacterial virulence and immune evasion.
  • The specific role of the capsular polysaccharide export protein (Wza) in CRAB virulence remains to be fully elucidated.

Purpose of the Study:

  • To investigate the virulence of the capsular polysaccharide export protein (Wza) in CRAB.
  • To determine the effect of Wza on capsule formation and its contribution to CRAB pathogenicity.
  • To analyze the impact of Wza on the expression of other genes involved in the Wzy capsule polysaccharide synthesis pathway.

Main Methods:

  • Construction of *wza* gene knockout and complementation strains of CRAB.
  • Assessment of bacterial virulence through *in vitro* adhesion assays (A549 cells), antiserum complement killing, and anti-oxidation experiments.
  • Evaluation of *in vivo* pathogenicity using *Galleria mellonella* and mouse infection models.
  • Analysis of *wzb*, *wzc*, and *wzi* gene expression levels using RT-PCR.

Main Results:

  • *wza* knockout strains exhibited significantly reduced adhesion to A549 cells, lower antiserum complement killing ability, and decreased mortality in *G. mellonella* and mouse models compared to wild-type (WT) strains.
  • Expression of *wzb*, *wzc*, and *wzi* genes was significantly downregulated in *wza* knockout strains.
  • Complementation of the *wza* gene restored virulence, adhesion, complement killing ability, and gene expression to WT levels.
  • Antioxidant capacity was only slightly decreased in *wza* knockout bacteria.

Conclusions:

  • Wza is a critical determinant of CRAB virulence, contributing to adhesion, immune evasion, and overall pathogenicity.
  • Wza influences the expression of other genes within the Wzy capsule polysaccharide synthesis pathway, affecting capsule assembly, export, and extracellular fixation.
  • Targeting Wza presents a potential strategy for combating CRAB infections by attenuating its virulence.