Differences in eucaryotic cell binding of Pseudomonas

Microb Pathog. 1994 Nov;17(5):291-9. doi: 10.1006/mpat.1994.1075.


The lungs of cystic fibrosis (CF) patients are frequently chronically colonized by Pseudomonas aeruginosa. Recently there has been an increase in colonization by another pathogen Pseudomonas cepacia, which can cause a rapid decline in clinical condition or death of the patient. The nature of the factor(s) which predispose CF patients to colonization by one or both of these opportunistic pathogens is unknown. It has been suggested that the genetic defect in CF patients results in an increase in the number of epithelial cell receptors available to P. aeruginosa in the lung, thus rendering CF patients more susceptible to bacterial colonization than non-CF individuals. In this study, we have examined adherence of several strains of P. aeruginosa and P. cepacia to a variety of continuous cell lines, as well as primary cultures of CF and non-CF nasal polyp cells. The results suggested that there may be a decrease in the number of receptors available to both strains of Pseudomonas on cells of canine origin compared to human cells. Both strains appear to use pili as the primary adhesin, but there is also evidence that non-pilus adhesins contribute significantly to eucaryotic cell binding. P. cepacia exhibited microcolony formation on all cell types, which is typical of the localized adherence pattern characteristic of the enteropathogenic Escherichia coli. However, we were unable to demonstrate, with either P. cepacia or P. aeruginosa, a significant increase in adherence to CF compared to non-CF nasal polyp cultures.(ABSTRACT TRUNCATED AT 250 WORDS)

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adhesins, Bacterial
  • Animals
  • Bacterial Adhesion / physiology*
  • Burkholderia cepacia / pathogenicity
  • Burkholderia cepacia / physiology*
  • Cell Line
  • Cystic Fibrosis / microbiology*
  • Dogs
  • Eukaryotic Cells
  • Fimbriae, Bacterial / physiology
  • Humans
  • Nasal Polyps / microbiology*
  • Pseudomonas aeruginosa / pathogenicity
  • Pseudomonas aeruginosa / physiology*


  • Adhesins, Bacterial