Lewis antigen expression and other pathogenic factors in the presence of atrophic chronic gastritis in a European population.

Abstract

To study the relationship between Helicobacter pylori cagA and vacA status and the expression of Lewis (Le) antigens and between these characteristics and atrophic chronic gastritis (ACG), H. pylori infection was assessed by culture and by histologic and serologic tests, cagA and vacA were assessed by a polymerase chain reaction--based reverse hybridization assay, and bacterial Le expression was assessed by immunoblotting. ACG was any form of antral or fundic atrophy with or without intestinal metaplasia. Of the 215 isolates, 64% were cagA(+) and 100% were vacA(+) (s1m1, 42%; s1m2, 29%; s2m2, 29%; and s2m1, 0). Le typing of 155 isolates showed that 6 (4%) were Le(x), 31 (20%) were Le(y), 87 (56%) were Le(x,y), and 31 (20%) were neither Le(x) nor Le(y). Two main clusters of isolates were identified by multiple correspondence analysis: s1a/m1/cagA(+)/Le(x)+/Le(y)+ (n=44; 29.7%) and s2/m2a/cagA(-)/Le(y)+ or Le(x)-/Le(y)- (n=29; 19.7%). Among patients with ACG, 54% of their isolates were from cluster s1m1/cagA(+)/Le(x)+/Le(y)+, which was associated with the presence of ACG (odds ratio, 7.4; 95% confidence interval, 1.5-37.0).