Antigenic mimicry between Helicobacter pylori and gastric mucosa in the pathogenesis of body atrophic gastritis

Negrini, R.; Savio, Antonella; Poiesi, Claudio; Bj, Appelmelk; Buffoli, Federico; Paterlini, A; Cesari, P.; Graffeo, M; Vaira, Dolorès; Franzin, G.

doi:10.1053/gast.1996.v111.pm8780570

Cited by 289 publications

(207 citation statements)

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“…The following murine immunoglobulin M monoclonal antibodies (MAbs) were used: MAb 54.1F6A, specific for Lewis x (G. van Dam, Leiden, The Netherlands [25]); MAb 1E52, specific for Lewis y (R. Negrini, Brescia, Italy [1,17,18]); MAb 19-O-Le, specific for H type 2 and Lewis y (Bioprobe, Amstelveen, The Netherlands [1]); MAb 4D2, specific for H type 1 (R. Negrini [1,17,18]); and MAb NAM61-1A2, specific for i antigen (D. Blanchard, Nantes, France [5]). MAbs specific for Lewis x did not cross-react with H type 2/Lewis y or vice versa; the anti-i MAb did not react with Lewis x, H type 2, or Lewis y.…”

Section: Methodsmentioning

confidence: 99%

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Phase Variation in Helicobacter Pylori Lipopolysaccharide

Appelmelk¹,

Vandenbrouck-Grauls²

2003

Antigenic Variation

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Section: Methodsmentioning

confidence: 99%

“…The identity of these LPS epitopes with molecules of the host may play a role in the induction of H. pylori-associated autoantibodies (1,17,18) and facilitate persistence in the gastric niche of humans (31).…”

mentioning

confidence: 99%

Phase Variation in Helicobacter Pylori Lipopolysaccharide

Appelmelk¹,

Vandenbrouck-Grauls²

2003

Antigenic Variation

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“…pylori infection gives rise to chronic inflammation, glandular atrophy and intestinal metaplasia in the gastric mucosa. [20][21][22] Jaskiewicz et al 23 reported that male subjects over 40 years of age are likely to demonstrate antral glandular atrophy, and patchy or diffuse intestinal metaplasia. With regard to glandular atrophy and intestinal metaplasia of the background mucosa, our young patients were mostly infected by H. pylori, however, they had less degree of corporal glandular atrophy and less frequent intestinal metaplasia around the intramucosal gastric cancer than elderly patients did.…”

Section: Intramucosal Gastric Cancer In the Youngmentioning

confidence: 99%

Intramucosal gastric adenocarcinoma of poorly differentiated type in the young is characterized by Helicobacter pylori infection and antral lymphoid hyperplasia

et al. 2007

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The aim of this investigation was to clarify the histological characteristics of gastric cancer in the young. Twenty-three surgically resected specimens of young patients (under 30 years of age; young group) with intramucosal cancer of poorly differentiated type and 42 surgically resected specimens of elderly patients (more than 40 years of age; elderly group) with tumors of the identical depth and histological type were examined. The degree of gastritis and Helicobacter pylori (H. pylori) infection was evaluated according to the updated Sydney system. The incidence of H. pylori infection was significantly higher in the young group than in the elderly group (96 vs 36%, Po0.05). Within the background mucosa, antral chronic inflammatory infiltrates with lymphoid-follicle hyperplasia were more severe, and intestinal metaplasia was less frequent in the young group than in the elderly group. Glandular atrophy was not different between the two groups. Intramucosal gastric adenocarcinomas of poorly differentiated type in the young may be associated with H. pylori infection with antral chronic inflammation with lymphoid-follicle hyperplasia, regardless of the existence of intestinal metaplasia within the background gastric mucosa.

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“…Moreover, a cross mimicry between bacterial and host antigens exist in H. pylori infected patients (Negrini et al 1996). Therefore, a pathogenetic link between H. pylori infection and diseases characterized by activation of inflammatory mediators and/or induction of autoimmunity might exist.…”

confidence: 99%