Helicobacter pylori does not require Lewis X or Lewis Y expression to colonize C3H/HeJ mice

Abstract

Helicobacter pylori strains frequently express Lewis X (Le(x)) and/or Le(y) on their cell surfaces as constituents of the O antigens of their lipopolysaccharide molecules. To assess the effect of Le(x) and Le(y) expression on the ability of H. pylori to colonize the mouse stomach and to adhere to epithelial cells, isogenic mutants were created in which fucT1 alone or fucT1 and fucT2, which encode the fucosyl transferases necessary for Le(x) and Le(y) expression, were deleted. C3H/HeJ mice were experimentally challenged with either wild-type 26695 H. pylori or its isogenic mutants. All strains, whether passaged in the laboratory or recovered after mouse passage, colonized the mice well and without consistent differences. During colonization by the mutants, there was no reversion to wild type. Similarly, adherence to AGS and KatoIII cells was unaffected by the mutations. Together, these findings indicate that Le expression is not necessary for mouse gastric colonization or for H. pylori adherence to epithelial cells.

FIG. 1.

Serum IgG responses to H. pylori whole-cell antigens in C3H/HeJ mice following challenge with wild-type (▪) and isogenic ΔfucT2 (•) and ΔfucT1/2 (▴) mutant mouse-passaged H. pylori strains. ×, negative control. Error bars indicate standard deviations. ODU, optical density units.

FIG. 2.

Binding of H. pylori strains to gastric epithelial cells (AGS-NY2 [A and C] and KatoIII [B and D]). Each panel compares binding of wild-type strain 26695 (solid lines) with that of its isogenic ΔfucT2 (A and B) or ΔfucT1/2 (C and D) mutant (dashed lines). Bacteria/cell ratios ranged from 1:1 to 1:100, and binding was estimated as the mean fluorescence intensity (MFI) by flow cytometry. Results are representative of those from two separate experiments.