title: Relation between clinical presentation, Helicobacter pylori density, interleukin 1beta and 8 production, and cagA status.
abstract: BACKGROUND
  It is not known whether cagA+ Helicobacter pylori in duodenal ulcer (DU) have enhanced virulence compared with non-DU cagA+ H pylori.
  
  
  OBJECTIVE
  To investigate the relation between presentation, H pylori density, interleukin 1beta (IL-1beta) and IL-8 production, and cagA status.
  
  
  METHODS
  Fifty DU and 50 gastritis patients with cagA+ H pylori and 11 with cagA- infections were studied. Bacterial density and cytokine production were assessed using the same biopsies. Cytokine production was also measured from supernatants of medium following coculture of H pylori with MKN-45 cells.
  
  
  RESULTS
  There was no relation between H pylori density and cagA status. There was a dose dependent relation between mucosal cytokine levels and density of cagA+ H pylori. H pylori density increased to a threshold, followed by a rapid increase in cytokines and then a plateau. IL-1beta and IL-8 levels in the antrum were greater in DU than in gastritis; in the corpus the cytokine level/H pylori differed irrespective of similar H pylori densities. However, cytokine production was similar in vitro, independent of presentation or biopsy site, suggesting that host factors are critical determinants of the inflammatory response. Mucosal IL-8 and IL-1beta levels were low with cagA- and cagA+, cagE- H pylori infections.
  
  
  CONCLUSIONS
  The increase in antral IL-1beta and IL-8 production and inflammation in DU is related to increased numbers of bacteria and not to an increase in cytokine production per cagA+ isolate. There was no evidence of enhanced virulence of H pylori from DU compared with cagA+ non-DU H pylori.
authors.affiliation: Department of Medicine, Veterans Affairs Medical Centre and Baylor College of Medicine, Houston, Texas, USA.
authors.forename: Y
authors.initials: Y
authors.lastname: Yamaoka
authors.forename: T
authors.initials: T
authors.lastname: Kodama
authors.forename: M
authors.initials: M
authors.lastname: Kita
authors.forename: J
authors.initials: J
authors.lastname: Imanishi
authors.forename: K
authors.initials: K
authors.lastname: Kashima
authors.forename: D Y
authors.initials: DY
authors.lastname: Graham
mesh_terms: D000328:Adult; D000942:Antigens, Bacterial; D001426:Bacterial Proteins / Q000235:genetics*; D001706:Biopsy; D004381:Duodenal Ulcer / Q000378:metabolism / Q000382:microbiology* / Q000473:pathology; D005260:Female; D005756:Gastritis / Q000378:metabolism / Q000382:microbiology / Q000473:pathology; D005838:Genotype; D016481:Helicobacter Infections / Q000150:complications* / Q000378:metabolism / Q000382:microbiology; D016480:Helicobacter pylori / Q000235:genetics / Q000302:isolation & purification* / Q000472:pathogenicity; D006801:Humans; D007375:Interleukin-1 / Q000096:biosynthesis; D016209:Interleukin-8 / Q000096:biosynthesis; D007378:Interleukins / Q000096:biosynthesis*; D008297:Male; D008875:Middle Aged; D016133:Polymerase Chain Reaction; D014407:Tumor Cells, Cultured; D014774:Virulence
chemical_list: D000942:Antigens, Bacterial; D001426:Bacterial Proteins; D007375:Interleukin-1; D016209:Interleukin-8; D007378:Interleukins; C080866:cagA protein, Helicobacter pylori