title: Presence of iceA1 but not cagA, cagC, cagE, cagF, cagN, cagT, or orf13 genes of Helicobacter pylori is associated with more severe gastric inflammation in Taiwanese.
abstract: OBJECTIVE
  The presence of the cag pathogenicity island (PAI) may enhance the virulence of Helicobacter pylori. This study determined the prevalence of genotypes of the PAI, IS605, and iceA1 in H. pylori strains in Taiwanese and whether these genotypes were related to the type of clinical disease or gastric pathology.
  
  
  METHODS
  One hundred clinical isolates were collected from 33 duodenal ulcer, 41 nonulcer related dyspepsia, 14 gastric ulcer, and 12 gastric malignancy patients. Polymerase chain reaction (PCR) assays were performed for cagA, cagC, cagE, cagF, and cagN in the cagI region, cagT and orf13 in the cagII region, and IS605 and iceA1 in all H. pylori isolates. Gastric histology of the infected host was reviewed using the updated Sydney system.
  
  
  RESULTS
  All strains were positive for all the selected genes in the PAI. PCR amplification found IS605 in 17%, while colony hybridization revealed it in 36% of strains. The prevalence of the cagA gene detected by PCR using cagA1, cagA2, and cagA3 primers was 26, 100, and 100%, respectively. The iceA1 gene existed in 72% of the H. pylori isolates. The mean ulcer size and the severity of acute gastric inflammation in patients infected with iceA1-positive strains were significantly greater than in those infected with iceA1-negative strains (p < 0.05).
  
  
  CONCLUSIONS
  All clinical H. pylori isolates from different gastric diseases in our Taiwanese patients were positive for the PAI, but only 36% of these isolates carried an IS605 insertion. The selected genes in the PAI were not correlated with disease outcome. The determination of cagA prevalence is based on the selection of suitable primers. In contrast, bacterial factors such as the presence of iceAl could be related to severity of gastric inflammation and increase in ulcer size in H. pylori-infected patients.
authors.affiliation: Department of Microbiology and Immunology, National Cheng Kung University Medical College, Tainan, Taiwan.
authors.forename: Shew-Meei
authors.initials: SM
authors.lastname: Sheu
authors.forename: Bor-Shyang
authors.initials: BS
authors.lastname: Sheu
authors.forename: Hsiao-Bai
authors.initials: HB
authors.lastname: Yang
authors.forename: Ching
authors.initials: C
authors.lastname: Li
authors.forename: Tro-Chen
authors.initials: TC
authors.lastname: Chu
authors.forename: Jiunn-Jong
authors.initials: JJ
authors.lastname: Wu
mesh_terms: D000942:Antigens, Bacterial / Q000235:genetics*; D001426:Bacterial Proteins / Q000235:genetics*; D004251:DNA Transposable Elements / Q000235:genetics; D004415:Dyspepsia / Q000382:microbiology; D005753:Gastric Mucosa / Q000473:pathology*; D005756:Gastritis / Q000382:microbiology / Q000473:pathology*; D016481:Helicobacter Infections / Q000382:microbiology / Q000473:pathology*; D016480:Helicobacter pylori / Q000235:genetics* / Q000472:pathogenicity; D006801:Humans; D010437:Peptic Ulcer / Q000382:microbiology; D013274:Stomach Neoplasms / Q000382:microbiology; D013624:Taiwan; D014774:Virulence / Q000235:genetics
chemical_list: D000942:Antigens, Bacterial; D001426:Bacterial Proteins; D004251:DNA Transposable Elements; C405087:iceA1 protein, Helicobacter pylori