ABH and Lewis histo-blood group antigens, a model for the meaning of oligosaccharide diversity in the face of a changing world

Marionneau, Séverine; Cailleau-Thomas, Anne; Rocher, Jézabel; Moullac-Vaidye, Béatrice Le; Ruvoën, Nathalie; Clément, Michel; Pendu, Jacques Le

doi:10.1016/s0300-9084(01)01321-9

Cited by 288 publications

(276 citation statements)

References 68 publications

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“…ABO blood group antigens present in human intestinal mucous can serve as receptors for a wide range of pathogens such as Helicobacter pylori (36) and Campylobacter jejuni (37). Subtle differences in glycan structure, density, and presentation can be the deciding factors between resistance and susceptibility.…”

Section: Discussionmentioning

confidence: 99%

The Caenorhabditis elegansbus-2 Mutant Reveals a New Class of O-Glycans Affecting Bacterial Resistance

Palaima

Leymarie

Stroud

et al. 2010

Journal of Biological Chemistry

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Microbacterium nematophilum causes a deleterious infection of the C. elegans hindgut initiated by adhesion to rectal and anal cuticle. C. elegans bus-2 mutants, which are resistant to M. nematophilum and also to the formation of surface biofilms by Yersinia sp., carry genetic lesions in a putative glycosyltransferase containing conserved domains of core-1 ␤1,3-galactosyltransferases. bus-2 is predicted to act in the synthesis of core-1 type O-glycans. This observation implies that the infection requires the presence of host core-1 O-glycoconjugates and is therefore carbohydrate-dependent. Chemical analysis reported here reveals that bus-2 is indeed deficient in core-1 O-glycans. These mutants also exhibit a new subclass of O-glycans whose structures were determined by high performance tandem mass spectrometry; these are highly fucosylated and have a novel core that contains internally linked GlcA. Lectin studies showed that core-1 glycans and this novel class of O-glycans are both expressed in the tissue that is infected in the wild type worms. In worms having the bus-2 genetic background, core-1 glycans are decreased, whereas the novel fucosyl O-glycans are increased in abundance in this region. Expression analysis using a red fluorescent protein marker showed that bus-2 is expressed in the posterior gut, cuticle seam cells, and spermatheca, the first two of which are likely to be involved in secreting the carbohydraterich surface coat of the cuticle. Therefore, in the bus-2 background of reduced core-1 O-glycans, the novel fucosyl glycans likely replace or mask remaining core-1 ligands, leading to the resistance phenotype. There are more than 35 Microbacterium species, some of which are pathogenic in man. This study is the first to analyze the biochemistry of adhesion to a host tissue by a Microbacterium species.

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Section: Discussionmentioning

confidence: 99%

The Caenorhabditis elegansbus-2 Mutant Reveals a New Class of O-Glycans Affecting Bacterial Resistance

Palaima

Leymarie

Stroud

et al. 2010

Journal of Biological Chemistry

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“…The rabbit-RHDV system can be paralleled with that of noroviruses, another genus from the Caliciviridae family causing gastro-enteretis in humans. It has been shown that the susceptibility or resistance to noroviruses depends on the presence of fucoses on the surface of epithelial cells, under the control of a polymorphic genetic system (Marionneau et al, 2001). As a result, most strains of the virus can only infect a given genetic subset of the human population (Le Pendu et al, 2006;Tan and Jiang, 2005).…”

Section: Introductionmentioning

confidence: 99%

Evolution of microparasites in spatially and genetically structured host populations: The example of RHDV infecting rabbits

Fouchet

Pendu

Jean

et al. 2009

Journal of Theoretical Biology

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A c c e p t e d m a n u s c r i p t 2 AbstractSeveral studies have shown that classical results of microparasite evolution could not extend to the case where the host species shows an important spatial structure. Rabbit Haemorrhagic Disease Virus (RHDV), responsible for Rabbit Haemorrhagic Disease (RHD), which recently emerged in rabbits, has strains within a wide range of virulence, thus providing an interesting example of competition between strains infecting a host species with a metapopulation structure. In addition, rabbits may show a genetic diversity regarding RHDV susceptibility. In the present paper we use the example of the rabbit-RHDV interaction to study the competition between strains of a same microparasite in a host population that is both spatially and genetically structured. Using metapopulation models we show that the evolution of the microparasite is guided by a trade-off between its capacity to invade subpopulations potentially infected by other strains and its capacity to persist within the subpopulation. In such a context, host genetic diversity acts by reducing the number of hosts susceptible to each strain, often favouring more persistent -and generally less virulent -strains. We also show that even in a stochastic context where host genes regularly go locally extinct, the microparasite pressure helps maintain the genetic diversity in the long term while reinforcing gene loss risk in the short term. Finally, we study how different demographic and epidemiologic parameters affect the coevolution between the rabbit and RHDV.

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“…The first, a bacterial pathogen, adapts through accumulated mutations to exploit common host phenotypes and creates frequency-dependent selection in favour of rarer ABO alleles. Several precedents for bacterial-pathogen adaptation to different glycosylated host structures have been described (Karlsson 1998;Marionneau et al 2001). Such pathogens generate polymorphism under a wide range of conditions but fail to explain the frequency distribution of ABO phenotypes.…”

Section: Introductionmentioning

confidence: 99%

Evolution of the human ABO polymorphism by two complementary selective pressures

Seymour

Allan

Pomiankowski

et al. 2004

Proc. R. Soc. Lond. B

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The best-known example of terminal-glycan variation is the ABO histo-blood group polymorphism in humans. We model two selective forces acting on histo-blood group antigens that may account for this polymorphism. The first is generated by the invasion of opportunistic bacterial or other pathogens that interact with the epithelial-mucosal surfaces. The bacteria adapt to the microenvironments of common host phenotypes and so create frequency-dependent selection for rarer host alleles. The second is generated by intracellular viruses, and accounts for the observed differentials between the ABO-phenotype frequencies. It is thought that viruses acquire histo-blood group structures as part of their envelope from their previous host. The presence of host antigens on the viral envelope causes differential transmission of the virus between host types owing to the asymmetric action of ABO natural antibodies. Our model simulations show that these two forces acting together can account for the major features of the ABO polymorphism in humans.

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ABH and Lewis histo-blood group antigens, a model for the meaning of oligosaccharide diversity in the face of a changing world

Cited by 288 publications

References 68 publications

The Caenorhabditis elegansbus-2 Mutant Reveals a New Class of O-Glycans Affecting Bacterial Resistance

The Caenorhabditis elegansbus-2 Mutant Reveals a New Class of O-Glycans Affecting Bacterial Resistance

Evolution of microparasites in spatially and genetically structured host populations: The example of RHDV infecting rabbits

Evolution of the human ABO polymorphism by two complementary selective pressures

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