| Autor: |
Heneghan, Michael A, Moran, Anthony P, Feeley, Kenneth M, Egan, Ernest L, Goulding, Joseph, Connolly, Charles E, McCarthy, Ciaran F |
| Zdroj: |
FEMS Immunology and Medical Microbiology; April 1998, Vol. 20 Issue: 4 p257-266, 10p |
| Abstrakt: |
The Lewisbblood group antigen has been implicated as a putative receptor for Helicobacter pyloriin the gastric mucosa. Furthermore, an increased prevalence of duodenal ulcer was found in non‐secretors and it has been suggested that secretor status may influence bacterial colonisation density. Other investigators have hypothesised that severity of antral gastritis may be related to colonisation density of the bacterium alone, and that a critical bacterial load is necessary for the development of duodenal ulcer. Our objectives were to investigate whether a relationship existed between host Lewis and ABO blood group phenotype and prevalence of H. pyloriinfection. In addition we investigated whether bacterial colonisation density and the ensuing inflammatory response was influenced by secretor status and ABO blood group phenotype. The Lewis and ABO blood group phenotype of 207 patients undergoing upper endoscopy was determined. Of these, 136 were secretors and 62 were non‐secretors. Forty‐five percent of patients were infected with H. pylori. No significant association was found between H. pyloriinfection and expression of Lewisaor Lewisbblood group antigen. The mean histological density of H. pyloriwas 1.8±0.2 among non‐secretors and 1.51±0.13 among secretors (P=0.209), with a mean grade of lymphocytic infiltration significantly greater in H. pylori‐infected non‐secretors (2.23±0.123 vs 1.8±0.074; P=0.003). In addition, blood group O non‐secretors had a significantly higher grade of lymphocyte infiltration of their gastric mucosa compared to non‐O non‐secretors (2.53±0.133 vs 1.93±0.181, P=0.027). These results suggest that although no in vivo relationship exists between H. pyloriand preferential adhesion to the putative Lewisbreceptor, bacterial colonisation and the ensuing inflammatory response may be influenced at least in part by host expression of ABO and Lewisablood group antigens. |
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