Mannose-binding lectin deficiency does not increase the prevalence of Helicobacter pylori seropositivity

Abstract

Background Mannose-binding lectin is an immune molecule that can bind to pathogens and initiate the complement cascade. In certain clinical situations, often characterized by immune compromise, mannose-binding lectin deficiency can increase the risk of infectious complications. Helicobacter pylori is one of the most common human infections and can bind mannose-binding lectin. Therefore, we examined whether mannose-binding lectin status influences the prevalence of H. pylori infection.

Methods Two distinct populations were targeted. The first consisted of 166 volunteer blood donors, the second included 108 peripheral blood stem cell donors. All were tested for serological evidence of H. pylori infection, and had their mannose-binding lectin status characterized by genotyping, and quantification of mannose-binding lectin mannan-binding level and C4-deposition function in plasma.

Results H. pylori positive blood donors had higher blood mannose-binding lectin levels, as measured by C4 deposition (median 0.67 vs. 0.40, P=0.009, hazard ratio 2.82, 95% confidence interval 1.29–6.19) and mannan-binding assays (median 1.83 vs. 1.26, P=0.02, hazard ratio 1.28, 95% confidence interval 1.03–1.59). A trend was also found between the presence of an MBL2 coding mutation and a reduced prevalence of H. pylori. No significant associations were found in the second population.

Conclusions Mannose-binding lectin deficiency does not increase the risk of H. pylori infection. The finding in one population that greater mannose-binding lectin activity might predispose to infection, suggests that this study should be repeated in other large cohorts of normal subjects.