title: Colony variation of Helicobacter pylori: pathogenic potential is correlated to cell wall lipid composition.
abstract: BACKGROUND
  Differences in expression of disease after infection with Helicobacter pylori have so far been connected with host factors and bacterial interstrain variation. In this study, spontaneous and ecology-mediated intrastrain variation was examined.
  
  
  METHODS
  Four clinical isolates of H. pylori were shown to give rise to two colony forms. Bacterial morphology was examined by electron microscopy. Bacterial fractions were examined for proteins using ion exchange chromatography and SDS-PAGE; for lipids using thin-layer chromatography, lipid anion-exchange chromatography, column chromatography on silica gel, 31P-NMR, gas chromatography and mass spectrometry. Bacterial in vitro invasiveness and adhesiveness were examined in two different systems, and urease and VacA toxin were assayed by Western blot analysis.
  
  
  RESULTS
  H. pylori was shown to give rise to two colony forms: at normal pH the population was dominated by L colonies. One strain was chosen for further studies. Bacteria from L colonies retained VacA toxin and urease, did not invade or adhere to epithelial cells, and contained normal quantities of phosphatidylethanolamine. In a small frequency, spontaneous S colonies were formed. Bacteria from these colonies released VacA and urease, adhered to and invaded epithelial cells and contained increased amounts of lysophosphatidyl ethanolamine and phosphatidyl serine. After addition of HCl to the culture medium (pH6), almost only S colonies were formed. The results demonstrate that environmental factors, such as HCl, can change the bacterial cell wall, and thereby enhance expression of virulence factors of H. pylori in vitro. A similar in vivo variation would have implications for our understanding of the interaction between HCl secretion in the gastric mucosa and H. pylori in the development of peptic ulcer disease.
authors.affiliation: Institute of Medical Microbiology, University of Oslo, Norway.
authors.forename: G
authors.initials: G
authors.lastname: Bukholm
authors.forename: T
authors.initials: T
authors.lastname: Tannaes
authors.forename: P
authors.initials: P
authors.lastname: Nedenskov
authors.forename: Y
authors.initials: Y
authors.lastname: Esbensen
authors.forename: H J
authors.initials: HJ
authors.lastname: Grav
authors.forename: T
authors.initials: T
authors.lastname: Hovig
authors.forename: S
authors.initials: S
authors.lastname: Ariansen
authors.forename: I
authors.initials: I
authors.lastname: Guldvog
mesh_terms: D001422:Bacterial Adhesion; D001426:Bacterial Proteins / Q000378:metabolism; D017358:Cell Wall Skeleton / Q000378:metabolism*; D002849:Chromatography, Gas; D015169:Colony Count, Microbial; D046508:Culture Techniques; D003603:Cytotoxins / Q000378:metabolism; D005753:Gastric Mucosa / Q000378:metabolism / Q000382:microbiology* / Q000473:pathology; D016481:Helicobacter Infections / Q000378:metabolism / Q000382:microbiology* / Q000473:pathology; D016480:Helicobacter pylori / Q000378:metabolism / Q000472:pathogenicity* / Q000648:ultrastructure; D006801:Humans; D008246:Lysophospholipids / Q000378:metabolism; D013058:Mass Spectrometry; D008855:Microscopy, Electron, Scanning; D010743:Phospholipids / Q000378:metabolism*; D014510:Urease / Q000378:metabolism
chemical_list: D001426:Bacterial Proteins; D017358:Cell Wall Skeleton; D003603:Cytotoxins; D008246:Lysophospholipids; D010743:Phospholipids; C074689:VacA protein, Helicobacter pylori; C008301:lysophosphatidylethanolamine; D014510:Urease