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Journal of Clinical Microbiology, January 2002, p. 227-232, Vol. 40, No. 1
0095-1137/02/$04.00+0 DOI: 10.1128/JCM.40.1.227-232.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.
Torkel Wadström,2 Marika Mikelsaar,4 Paul W. OToole,5 John Telford,6 Lars Engstrand,7 Shigeru Kamiya,8 Andreas F. Mentis,9 and Anthony P. Moran1*
Department of Microbiology, National University of Ireland, Galway, Ireland,1 Department of Medical Microbiology, Dermatology and Infection, University of Lund, Lund,2 Epidemiology Unit of Digestive Diseases, Laboratory of Bacteriology, University of Victor Segalen Bordeaux 2, Bordeaux, France,3 Department of Medical Microbiology, University of Tartu, Tartu, Estonia,4 Institute of Molecular BioSciences, Massey University, Palmerston North, New Zealand,5 Department of Molecular Biology, Chiron Vaccines, Immunobiological Research Institute, Siena, Italy,6 Swedish Institute for Infectious Disease Control, Solna, Sweden,7 Department of Infectious Diseases, Kyorin University School of Medicine, Tokyo, Japan,8 Laboratory of Bacteriology, Hellenic Pasteur Institute, Athens, Greece9
Received 31 May 2001/ Returned for modification 15 August 2001/ Accepted 15 October 2001
A total of 309 Helicobacter pylori isolates from 18 different countries were analyzed with a previously developed lectin typing system. The system was developed by using a proteolytic pretreatment to enhance the carbohydrate fraction of the sample. Four lectins from Ulex europaeus, Lotus tetragonolobus, Erythrina cristigali, and Triticum vulgaris were used to type the strains. The lectins were chosen for their specificities for sugars commonly encountered in the lipopolysaccharide of H. pylori. The isolates were received from their parent institutions as pellets of biomass and were typed at one of three centers (in Ireland, Sweden, and Estonia). All 16 possible lectin reaction patterns were observed in the study, with the isolates with the predominant pattern exhibiting reactions with all the lectins in the panel. For European patients suffering from gastritis, an association was noted between lectin reaction pattern MH4 and atrophic chronic gastritis; isolates with lectin reaction pattern MH4 were isolated from patients with atrophic chronic gastritis, whereas isolates with this pattern were not isolated from patients with chronic gastritis (P = 0.0006). In addition, statistically significant relationships were noted between the lectin reaction pattern and the associated pathology of isolates from the Swedish population. Isolates with patterns MH13 and MH16, which had low lectin reactivities, correlated with nonulcer disease (P = 0.0025 and P = 0.0002, respectively), and all four isolates from adenocarcinoma patients were characterized as possessing reaction pattern MH16. In contrast, isolates with lectin reaction patterns MH1 and MH10, which had high lectin reactivities, were associated with ulcer disease (P = 0.046 and P = 0.0022, respectively).
See the Appendix for the members of the Eurohepygast Study Group.
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