The relationship between O-chain expression and colonisation ability of Helicobacter pylori in a mouse model

Abstract

The influence of lipopolysaccharide (LPS) O-polysaccharide chain production on the colonisation ability of Helicobacter pylori in four mouse models (NMRI, C57BL/6, CBA/Ca, and BALB/cA mice) was studied. H. pylori strains that produced smooth-form LPS (S-LPS) detectable in silver-stained electrophoretic gels colonised mice. In contrast, a laboratory-passaged strain G50 and the culture collection strain CCUG 17874 did not colonise mice; the former strain produced low amounts of O-chains only detectable in immunoblotting but not in silver-stained gels, whereas the latter produced rough-form LPS (R-LPS) without O-chains. Furthermore, a galE isogenic mutant, which produced R-LPS, did not colonise mice. However, after repeated broth culture, strains G50 and CCUG 17874 produced S-LPS detectable in silver-stained gels and were capable of colonising mice. Consistent with the production of O-chains, all colonising strains produced Lewis (Le) antigens, Le(x) and/or Le(y). Except for low expression of Le(y) by non-colonising G50, reflecting low production of O-chains, all other non-colonising strains and the galE mutant lacked expression of Le antigens consistent with their production of R-LPS. Lectin typing of strains supported these findings, and also showed that lectin types did not differ before and after colonisation. The low level of O-chain production and Le antigen expression by the non-colonising G50 may not be sufficient to aid colonisation. Examination of protein profiles of H. pylori strains before inoculation showed that protein expression was not significantly different between colonising and non-colonising strains. These results show that S-LPS production with O-chain expression is required by H. pylori for colonisation in a number of mouse models and that care should be taken with inoculating H. pylori strains that loss of O-chains does not occur during subculturing.

Anti-Lewis X Antibody PromotesHelicobacter pyloriAdhesion to Gastric Epithelial Cells

“…Lewis (Le) blood group antigens are commonly present in the human gastric mucosa and are also expressed on the O-specific chain of the lipopolysaccharide (LPS) of H. pylori (4,5,18,24). The molecular mimicry between bacteria and host could be involved in colonization, adaptation to the host, the induction of autoreactive antibodies (Abs), or even gastric damage (3,19,20,21).…”

Helicobacter pyloriInduces Plasminogen Activator Inhibitor 2 in Gastric Epithelial Cells through Nuclear Factor-κB and RhoA

“…It seems, then, that H. pylori induction of PAI-2 occurs through different mechanisms in gastric epithelial cells compared with mononuclear cells. There are, however, strain differences in lipopolysaccharide (38), and additional work is needed to define precisely the bacterial factors regulating PAI-2 expression.…”

Phenotypic Variation ofHelicobacter pyloriIsolates from Geographically Distinct Regions Detected by Lectin Typing

“…They may act in the evasion of host defenses, and subsequently, due to the chronic nature of the infection, their expression may play a role in autoimmune aspects of pathology (22). Also, it has been suggested that these antigens act in adhesion of the bacterium to the gastric mucosa (2,7,21). Furthermore, it has been reported that the expression of these fucosylated blood group antigens by H. pylori is related to the host Le phenotype (33), suggesting that carbohydrate expression by the bacteria adapts to the host environment.…”