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The Pseudomonas aeruginosa flagellar cap protein, FliD, is responsible for mucin adhesion

S K Arora1, B W Ritchings, E C Almira

  • 1Department of Medicine/Infectious Diseases, University of Florida, Gainesville 32610, USA.

Infection and Immunity
|March 6, 1998
PubMed

Insights

Pseudomonas aeruginosa uses the flagellar cap protein FliD for mucin adhesion, crucial for airway colonization in cystic fibrosis. FliD

Area of Science:

  • Microbiology
  • Bacterial Pathogenesis
  • Molecular Biology

Background:

  • Pseudomonas aeruginosa mucin adhesion is critical for airway colonization in cystic fibrosis patients.
  • The initial colonization mechanisms of P. aeruginosa are not fully understood.

Purpose of the Study:

  • To investigate the role of the flagellar cap protein FliD in P. aeruginosa mucin adhesion.
  • To elucidate the regulatory mechanisms governing fliD gene expression.

Main Methods:

  • Construction of a polar chromosomal insertional mutation in the P. aeruginosa fliD gene.
  • In vitro mucin adhesion assays using mutated and wild-type P. aeruginosa.
  • In vitro competition experiments with purified FliD, PilA, and FlaG proteins.
  • Analysis of fliD gene transcription regulation using beta-galactosidase assays.

Main Results:

  • A fliD gene mutation rendered P. aeruginosa nonadhesive to mucin.
  • Restoration of adhesion by providing the fliD gene on a plasmid.
  • Purified FliD protein inhibited mucin adhesion of nonpiliated P. aeruginosa.
  • fliD gene transcription is independent of the sigma28 flagellar sigma factor.
  • FliD expression is regulated by FleQ and the sigma54 (RpoN) alternate sigma factor.

Conclusions:

  • The flagellar cap protein FliD is essential for Pseudomonas aeruginosa mucin adhesion.
  • FliD plays a significant role in the initial colonization of airways in cystic fibrosis.
  • The fliD gene exhibits unique transcriptional regulation by FleQ and sigma54 (RpoN).

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