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Infection and Immunity, February 2000, p. 937-941, Vol. 68, No. 2
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Relationship of Blood Group Determinants on Helicobacter pylori Lipopolysaccharide with Host Lewis Phenotype and Inflammatory Response

Michael A. Heneghan,1,2 Ciaran F. McCarthy,1 and Anthony P. Moran2,*

Department of Medicine, Clinical Science Institute, University College Hospital Galway,1 and Laboratory of Molecular Biochemistry, Department of Microbiology,2 National University of Ireland, Galway, Ireland

Received 14 May 1999/Returned for modification 28 July 1999/Accepted 8 November 1999

As Lewis a (Lea) and Lewis b (Leb) blood group antigens are isoforms of Lewis x (Lex) and Lewis y (Ley) and are expressed in the gastric mucosa, we evaluated whether the patterns of expression of Lex and Ley on Helicobacter pylori lipopolysaccharides reflected those of host expression of Lea and Leb. When 79 patients (secretors and nonsecretors) were examined for concordance between bacterial and host Le expression, no association was found (chi 2 = 5.734, 3 df, P = 0.125), nor was there a significant difference between the amount of Lex or Ley expressed on isolates from ulcer and chronic gastritis patients (P > 0.05). Also, the effect of host and bacterial expression of Le antigens on bacterial colonization and the observed inflammatory response was assessed. In ulcer patients, Lex expression was significantly related to neutrophil infiltration (rs = 0.481, P = 0.024), whereas in chronic gastritis patients significant relationships were found between Lex expression and H. pylori colonization density (rs = 0.296, P = 0.03), neutrophil infiltrate (rs = 0.409, P = 0.001), and lymphocyte infiltrate (rs = 0.389, P = 0.002). Furthermore, bacterial Ley expression was related to neutrophil (rs = 0.271, P = 0.033) and lymphocyte (rs = 0.277, P = 0.029) infiltrates. Thus, although no evidence of concordance was found between bacterial and host expression of Le determinants, these antigens may be crucial for bacterial colonization, and the ensuing inflammatory response appears, at least in part, to be influenced by Le antigens.

* Corresponding author. Mailing address: Laboratory of Molecular Biochemistry, Department of Microbiology, National University of Ireland, Galway, University Road, Galway, Ireland. Phone: 353-91-524411, ext. 3163. Fax: 353-91-525700. E-mail: anthony.moran{at}nuigalway.ie.

Infection and Immunity, February 2000, p. 937-941, Vol. 68, No. 2
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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