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. 2004 Feb;72(2):880-8.
doi: 10.1128/IAI.72.2.880-888.2004.

Evaluation of the association of nine Helicobacter pylori virulence factors with strains involved in low-grade gastric mucosa-associated lymphoid tissue lymphoma

Philippe Lehours  1 , Armelle Ménard, Sandrine Dupouy, Bernard Bergey, Fréderique Richy, Frank Zerbib, Agnès Ruskoné-Fourmestraux, Jean Charles Delchier, Francis Mégraud
Affiliations

Evaluation of the association of nine Helicobacter pylori virulence factors with strains involved in low-grade gastric mucosa-associated lymphoid tissue lymphoma

Philippe Lehours et al. Infect Immun. 2004 Feb.

Abstract

Helicobacter pylori has been associated with the development of two malignant diseases: gastric adenocarcinoma and gastric mucosa-associated lymphoid tissue (MALT) lymphoma. Although the cag pathogenicity island, especially the cagA gene, has been linked with adenocarcinoma, few data concerning H. pylori pathogenic factors involved in low-grade gastric MALT lymphoma are available. The goal of this study was to analyze the prevalence of and correlation between genes coding for seven H. pylori virulence factors (cagA, cagE, vacA, iceA, babA, hopQ, and oipA) and two novel adhesins (sabA and hopZ) by comparing a collection of 43 H. pylori strains isolated from patients with low-grade gastric MALT lymphoma to 39 strains isolated from age-matched patients with gastritis only. Our results show that taken individually, none of the nine genes tested can be considered associated with MALT strains and allow us to conclude that MALT pathogenesis is not linked with more proinflammatory H. pylori strains. We demonstrated that in patients infected with strains harboring the iceA1 allele, sabA functional status, and hopZ "off" status, the odds of developing a MALT lymphoma were 10 times higher. However, the low prevalence of such strains (10 of 43 MALT strains) renders this triple association a low-sensitivity marker for MALT strains. Our data confirmed that H. pylori virulence factors are correlated with one another. If the involvement of H. pylori in MALT lymphoma is well established, the pathomechanism by which gastric lymphoma occurs remains to be identified.

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Figures

FIG. 1.
FIG. 1.
Dendrogram of the distribution of 70 H. pylori strains from both strain populations for which complete data were available for all variables. Strains have been grouped according to cagA, cagE, vacA, babA, iceA, hopQ, oipA, hopZ, and sabA status.
FIG. 2.
FIG. 2.
MCA plot of 39 and 31 H. pylori strains isolated from patients suffering from gastric MALT lymphoma (A) and from gastritis (B), respectively, for which complete data were available according to cagA, cagE, vacA, babA, iceA, hopQ, oipA, hopZ, and sabA status.
FIG. 3.
FIG. 3.
Distribution of the strains harboring the group A and group B combinations among Helicobacter pylori strains isolated from patients with gastric MALT lymphoma or gastritis only.
FIG. 4.
FIG. 4.
Distribution of strains harboring the triple combination iceA1, sabA on, and hopZ off among H. pylori strains isolated from patients with gastric MALT lymphoma or gastritis only.
See this image and copyright information in PMC

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