Evidence for ethnic tropism of Helicobacter pylori

Typeset version

 

TY  - JOUR
  - Campbell, S. and Fraser, A. and Holliss, B. and Schmid, J. and O'Toole, P. W.
  - 1997
  - January
  - Infect Immun
  - Evidence for ethnic tropism of Helicobacter pylori
  - Validated
  - 65
  - 9
  - 3708
  - 12
  - Helicobacter pylori infection in humans is linked to gastritis, gastric and duodenal ulcers, and gastric cancer. Peptic ulcer disease, as distinct from chronic asymptomatic infection, is strongly associated with expression of bacterial virulence markers, including a major antigen, CagA, and the vacuolating cytotoxin VacA. We have previously described significant differences in colonization rates, independent of socioeconomic status, among ethnic groups in New Zealand. To evaluate relative risks for peptic ulcer disease, we examined the frequency of two virulence markers in H. pylori strains infecting these ethnic groups. Although these markers occurred significantly more frequently in strains isolated from Polynesians than in strains from Europeans, this frequency was not reflected in the incidence of peptic ulcer disease in the two groups. DNA fingerprinting of the urease gene showed that Polynesians are more frequently infected by a group of strains which are genetically distinct from those affecting European New Zealanders. Our data suggest that separate bacterial lineages may have evolved in parallel with race-specific specialization.
  - http://www.ncbi.nlm.nih.gov/pubmed/9284141
DA  - 1997/01
ER  - 
@article{V277480554,
   = {Campbell, S. and Fraser, A. and Holliss, B. and Schmid, J. and O'Toole, P. W.},
   = {1997},
   = {January},
   = {Infect Immun},
   = {Evidence for ethnic tropism of Helicobacter pylori},
   = {Validated},
   = {65},
   = {9},
  pages = {3708--12},
   = {{Helicobacter pylori infection in humans is linked to gastritis, gastric and duodenal ulcers, and gastric cancer. Peptic ulcer disease, as distinct from chronic asymptomatic infection, is strongly associated with expression of bacterial virulence markers, including a major antigen, CagA, and the vacuolating cytotoxin VacA. We have previously described significant differences in colonization rates, independent of socioeconomic status, among ethnic groups in New Zealand. To evaluate relative risks for peptic ulcer disease, we examined the frequency of two virulence markers in H. pylori strains infecting these ethnic groups. Although these markers occurred significantly more frequently in strains isolated from Polynesians than in strains from Europeans, this frequency was not reflected in the incidence of peptic ulcer disease in the two groups. DNA fingerprinting of the urease gene showed that Polynesians are more frequently infected by a group of strains which are genetically distinct from those affecting European New Zealanders. Our data suggest that separate bacterial lineages may have evolved in parallel with race-specific specialization.}},
   = {http://www.ncbi.nlm.nih.gov/pubmed/9284141},
  source = {IRIS}
}
AUTHORSCampbell, S. and Fraser, A. and Holliss, B. and Schmid, J. and O'Toole, P. W.
YEAR1997
MONTHJanuary
JOURNALInfect Immun
TITLEEvidence for ethnic tropism of Helicobacter pylori
STATUSValidated
PEER_REVIEW
SEARCH_KEYWORD
VOLUME65
ISSUE9
START_PAGE3708
END_PAGE12
ABSTRACTHelicobacter pylori infection in humans is linked to gastritis, gastric and duodenal ulcers, and gastric cancer. Peptic ulcer disease, as distinct from chronic asymptomatic infection, is strongly associated with expression of bacterial virulence markers, including a major antigen, CagA, and the vacuolating cytotoxin VacA. We have previously described significant differences in colonization rates, independent of socioeconomic status, among ethnic groups in New Zealand. To evaluate relative risks for peptic ulcer disease, we examined the frequency of two virulence markers in H. pylori strains infecting these ethnic groups. Although these markers occurred significantly more frequently in strains isolated from Polynesians than in strains from Europeans, this frequency was not reflected in the incidence of peptic ulcer disease in the two groups. DNA fingerprinting of the urease gene showed that Polynesians are more frequently infected by a group of strains which are genetically distinct from those affecting European New Zealanders. Our data suggest that separate bacterial lineages may have evolved in parallel with race-specific specialization.
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URLhttp://www.ncbi.nlm.nih.gov/pubmed/9284141
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