Host Lewis phenotype‐dependentHelicobacter pyloriLewis antigen expression in rhesus monkeys

Abstract

Both human and H. pylori populations are polymorphic for the expression of Lewis antigens. Using an experimental H. pylori challenge of rhesus monkeys of differing Lewis phenotypes, we aimed to determine whether H. pylori populations adapt their Lewis phenotypes to those of their hosts. After inoculation of four monkeys with a mixture of seven strains identified by RAPD-polymerase chain reaction, H. pylori Lewis expression was followed in 86 isolates obtained over 40 wk. Host Lewis(a/b) secretion status was characterized by immunological assays. Fingerprints of the predominating strain (J166) were identical in all four animals after 40 wk, but its Lewis phenotype had substantial variability in individual hosts. At 40 wk, J166 populations from two Lewis(a-b+) animals predominantly expressed Lewis(y). In contrast, J166 populations had switched to a Lewis(x) dominant phenotype in the two Lewis(a+b-) animals; a frame shift in futC, regulating conversion of Lewis(x) to Lewis(y), accounted for the phenotypic switch. The results indicate that individual cells in H. pylori populations can change Lewis phenotypes during long-term colonization of natural hosts to resemble those of their hosts, providing evidence for host selection for bacterial phenotypes.

Clinical Relevance and Diversity of Two Homologous Genes Encoding Glycosyltransferases in Helicobacter pylori

“…Pohl et al also showed that the variation in the ␤-(1,3)GalT gene homopolymeric tract length affected Le b expression (31). More importantly, using a Le b -expressing transgenic mouse model, they provided evidence that H. pylori can change the Le phenotype to match the Le phenotype of its host, supporting previous studies in humans and rhesus monkeys (31,38,39). The change to a type I Le phenotype was found to be linked to a variation in the ␤-(1,3)GalT gene homopolymeric tract length, suggesting that this locus is under host selection pressure (31).…”

Early-Life Family Structure and Microbially Induced Cancer Risk

“…pylori is especially so [42–44]. Passage through a host selects for particular genotypes [45], and the spreading of these genotypes to a genetically related host may lead to a better adapted [46], and thus more virulent, bacterial population than occurs when transmitted from an unrelated individual. An alternative hypothesis is that the observed phenomena reflect as-yet-unidentified cofactors associated with high birth order and large sibships; candidate factors include multiple H.…”

Alterations in Helicobacter pylori outer membrane and outer membrane vesicle-associated lipopolysaccharides under iron-limiting growth conditions*

“…It has been demonstrated previously that H. pylori LPS, especially the O-chain expression of Lewis antigens, is subject to environmental regulation in vitro 26,27 and in vivo, [28][29][30] and that H. pylori exhibits a growth phase-dependent response to iron starvation. 31 Although an influence of iron availability on bacterial expression of LPS has been reported in H. pylori cultures, 25 the effect of iron limitation on the LPS expressed on OMVs compared to bacterial cells has, to date, been unknown.…”