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Neisseria meningitidis undergoes PilC phase variation and PilE sequence variation during invasive disease

Anne Rytkönen1, Barbara Albiger, Paola Hansson-Palo

  • 1Microbiology and Tumor Biology Center, Karolinska Institutet, Stockholm, Sweden.

The Journal of Infectious Diseases
|January 28, 2004
PubMed

Insights

Neisseria meningitidis changes its surface proteins, like PilC, as it spreads from the upper respiratory tract to the blood and cerebrospinal fluid. This variation impacts bacterial adhesion and is key to invasive meningococcal disease.

Area of Science:

  • Microbiology
  • Infectious Diseases
  • Bacterial Pathogenesis

Background:

  • Neisseria meningitidis is a common upper respiratory tract (URT) colonizer.
  • Dissemination from the URT to the bloodstream and cerebrospinal fluid (CSF) can cause invasive meningococcal disease.
  • Bacterial surface protein expression can change during infection, influencing virulence.

Purpose of the Study:

  • To investigate changes in virulence-associated proteins of Neisseria meningitidis during dissemination.
  • To determine the role of PilC and PilE variations in bacterial adhesion and invasion.

Main Methods:

  • Isolation and characterization of Neisseria meningitidis strains from URT, blood, and CSF.
  • Analysis of phase variation in PilC and sequence variation in PilE.
  • Assessment of bacterial adhesion to human epithelial cells.

Main Results:

  • Bacteria from the URT showed better adhesion to epithelial cells than those from blood or CSF.
  • Phase variation in PilC and sequence variation in PilE were observed during dissemination.
  • PilC expression was frequent in serogroup B and URT strains but reduced in CSF strains.
  • Strains lacking PilC exhibited impaired adhesion.

Conclusions:

  • Neisseria meningitidis undergoes significant changes in virulence factors, including PilC phase variation and PilE sequence variation, during invasive disease progression.
  • PilC expression is crucial for bacterial adhesion to epithelial cells and likely plays a role in meningococcal pathogenesis.

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