Details

Autor(en) / Beteiligte

• Ryan, Kieran A
• Moran, Anthony P
• Hynes, Sean O
• Smith, Terry
• Hyde, Denise
• O′Morain, Colm A
• Maher, Majella

Titel

Genotyping of cagA and vacA, Lewis antigen status, and analysis of the poly-(C) tract in the α(1,3)-fucosyltransferase gene of Irish Helicobacter pylori isolates

Ist Teil von

• FEMS immunology and medical microbiology, 2000-06, Vol.28 (2), p.113-119

Ort / Verlag

Oxford, UK: Blackwell Publishing Ltd

Erscheinungsjahr

2000

Link zum Volltext

Quelle

Wiley Online Library Journals Frontfile Complete

Beschreibungen/Notizen

• Abstract Much work has focused on trying to identify markers in Helicobacter pylori that might allow the eventual disease outcome of an infection to be predicted. In this study we examined the cagA and vacA genotype, and Lewis status in a panel of 43 Irish H. pylori clinical isolates, and investigated a possible correlation with disease pathology. In addition, differences in the poly-(C) tract of the α(1,3)-fucosyltransferase gene were examined to identify a possible correlation with gene expression. Only three of 43 isolates were cagA-negative, whereas the remaining 40 isolates, independent of pathology, were cagA-positive. In all the strains we examined, the vacA signal-sequence was type s1a. For the vacA mid-region 12/43 isolates were type m1 and 31/43 isolates were type m2. These data, and examination of isolates from different pathology groups, suggests that there is no correlation between virulence and vacA genotype in the Irish population of H. pylori isolates. Western blotting of whole cell lysates from 32 H. pylori isolates showed 3/32 displayed only the Lex epitope, 12/32 only the Ley, 13/32 both epitopes and 4/32 neither epitope. No apparent association between Lewis phenotype and disease pathology was evident. A range of lengths of poly-(C) tract were observed in the α(1,3)-fucosyltransferase gene, however the length of the tract in an isolate did not correlate with the Lewis structures present. We conclude that future studies on H. pylori pathogenesis should not alone focus on the importance of molecular markers, but also on the host response, including genetic background and immune responsiveness.