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Lewis antigen expression in gastric mucosa of children: relationship with Helicobacter pylori infection
Authors:Nogueira Ana Margarida  Marques Terezinha  Soares Paula Cristina M  David Leonor  Reis Celso A  Serpa Jacinta  Queiroz Dulciene M  Rocha Gifone A  Rocha Andréia C
Affiliation:Department of Pathology, Federal University of Minas Gerais, Belo Horizonte, Brazil. anog@medicina.ufmg.br
Abstract:OBJECTIVE: Lewis epithelial antigen expression has a role in Helicobacter pylori adherence, presumably mainly in cagA-positive strains. The authors investigated whether Lewis antigen expression in children's gastric mucosa was associated with H. pylori infection, cagA status, patient age, or presence of duodenal ulcer (DU). METHODS: The expression of Lewis A (Le(a)), B (Le(b)), X (Le(x)), and Y (Le(y)) was detected by immunohistochemistry in the antral and oxyntic mucosae of 70 children. Children were divided in four age groups (<4 years; 4-8 years; 9-12 years; and 13-18 years). RESULTS: Forty-seven of the 70 children had H. pylori and 17 had DU. The cagA status was determined by polymerase chain reaction in 34 patients. Le(a) and Le(b) were expressed in 64% and 44% of the patients, respectively; Le(x) and Le(y) were expressed in the glands in all of the patients and in the superficial epithelium. Le(b) expression was more common among patients without H. pylori (15/23, 65%) than in those with H. pylori (16/47, 34%) (P = 0.03). In noninfected patients, Le(b) and superficial Le(y) expression were associated with increased age. Le(b) expression was more common in patients with chronic gastritis than in those with DU. Le(x) superficial expression was significantly associated with DU in patients with H. pylori. CONCLUSION: In children, the expression of Le(b) and Le(y) in the superficial gastric epithelium depends on age. Other receptors, such as Le(x), may have a role in H. pylori colonization, especially in patients with DU. Studies assessing the expression of Lewis antigens in children may contribute to an understanding of the mechanisms of acquisition of H. pylori infection.
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