The structure of the lipid anchor of<i>Campylobacter jejuni</i>polysaccharide

Corcoran, Adrian T.; Annuk, Heidi; Moran, Anthony P.

doi:10.1111/j.1574-6968.2006.00177.x

Cited by 20 publications

(22 citation statements)

References 32 publications

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“…This hypothesis is now complicated by the existence of the poly-Kdo linker. kpsC and kpsS mutants accumulate large aggregates of intracellular CPS (20,29), but there have been conflicting reports in the past as to whether the CPS is lipidated (18,31,33); here we provide evidence that these CPSs are not lipidated in E. coli. Notably, the intracellular aggregates from these mutants lack the characteristic membrane association seen in the aggregates of lipidated CPSs produced by export-deficient mutants (e.g., kpsT) (33).…”

Section: Discussionmentioning

confidence: 53%

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Conserved glycolipid termini in capsular polysaccharides synthesized by ATP-binding cassette transporter-dependent pathways in Gram-negative pathogens

Willis

Stupak

Richards

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

117

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Bacterial capsules are surface layers made of long-chain polysaccharides. They are anchored to the outer membrane of many Gram-negative bacteria, including pathogens such as Escherichia coli , Neisseria meningitidis , Haemophilus influenzae , and Pasteurella multocida . Capsules protect pathogens from host defenses including complement-mediated killing and phagocytosis and therefore represent a major virulence factor. Capsular polysaccharides are synthesized by enzymes located in the inner (cytoplasmic) membrane and are then translocated to the cell surface. Whereas the enzymes that synthesize the polysaccharides have been studied in detail, the structure and biosynthesis of the anchoring elements have not been definitively resolved. Here we determine the structure of the glycolipid attached to the reducing terminus of the polysialic acid capsular polysaccharides from E. coli K1 and N. meningitidis group B and the heparosan-like capsular polysaccharide from E. coli K5. All possess the same unique glycolipid terminus consisting of a lyso-phosphatidylglycerol moiety with a β-linked poly-(3-deoxy- d - manno -oct-2-ulosonic acid) (poly-Kdo) linker attached to the reducing terminus of the capsular polysaccharide.

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Section: Discussionmentioning

confidence: 53%

“…This lipid has been implicated in anchoring CPSs to the outer membrane (16). Mass spectrometry analysis of acid-hydrolyzed PSA from E. coli K1 and K92, as well as N. meningitidis group B, identified dipalmitoylglycerol as a component (17)(18)(19)(20). However, direct covalent linkage between the CPS and this lipid has not been established.…”

mentioning

confidence: 99%

Conserved glycolipid termini in capsular polysaccharides synthesized by ATP-binding cassette transporter-dependent pathways in Gram-negative pathogens

Willis

Stupak

Richards

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

117

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“…Subsequently, genomic analysis provided confirmation that the observed PSs of C. jejuni were capsule (CPSs; Parkhill et al, 2000). Corcoran et al (2006) demonstrated the phospholipid anchor in three CPS types (HS3, HS6, and HS23/36) was dipalmitoyl-glycerophosphate, with ester-linked hexadecanoic acids. Campylobacter species, like other Gram negative mucosal pathogens and unlike other enteric pathogens, express a CPS and lipooligosaccharide (LOS; core → lipid A) in lieu of a full length LPS (O-chain → core → lipid A).…”

Section: Campylobacter Capsules: Structures and Geneticsmentioning

confidence: 99%

Campylobacter Polysaccharide Capsules: Virulence and Vaccines

Guerry¹,

Poly²,

Riddle³

et al. 2012

Front. Cell. Inf. Microbio.

124

129

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Campylobacter jejuni remains a major cause of bacterial diarrhea worldwide and is associated with numerous sequelae, including Guillain Barré Syndrome, inflammatory bowel disease, reactive arthritis, and irritable bowel syndrome. C. jejuni is unusual for an intestinal pathogen in its ability to coat its surface with a polysaccharide capsule (CPS). These capsular polysaccharides vary in sugar composition and linkage, especially those involving heptoses of unusual configuration and O-methyl phosphoramidate linkages. This structural diversity is consistent with CPS being the major serodeterminant of the Penner scheme, of which there are 47 C. jejuni serotypes. Both CPS expression and expression of modifications are subject to phase variation by slip strand mismatch repair. Although capsules are virulence factors for other pathogens, the role of CPS in C. jejuni disease has not been well defined beyond descriptive studies demonstrating a role in serum resistance and for diarrhea in a ferret model of disease. However, perhaps the most compelling evidence for a role in pathogenesis are data that CPS conjugate vaccines protect against diarrheal disease in non-human primates. A CPS conjugate vaccine approach against this pathogen is intriguing, but several questions need to be addressed, including the valency of CPS types required for an effective vaccine. There have been numerous studies of prevalence of CPS serotypes in the developed world, but few studies from developing countries where the disease incidence is higher. The complexity and cost of Penner serotyping has limited its usefulness, and a recently developed multiplex PCR method for determination of capsule type offers the potential of a more rapid and affordable method. Comparative studies have shown a strong correlation of the two methods and studies are beginning to ascertain CPS-type distribution worldwide, as well as examination of correlation of severity of illness with specific CPS types.

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“…To solubilize released acylglycerols and diacylglycerols, the dried sample was extracted three times with 100 l of CHCl 3 /MeOH (1:1, v/v). This extract was then evaporated to dryness under a stream of nitrogen, and the components were peracetylated by treatment with 100 l of acetic anhydride, pyridine (1:1, v/v) at 86°C for 30 min (22). After cooling to room temperature, the reaction mixture was evaporated to dryness under a stream of nitrogen.…”

Section: Gas Chromatography/mass Spectrometry (Gc-ms) Analysis Of Fatmentioning

confidence: 99%

The Lipid A from Vibrio fischeri Lipopolysaccharide

Phillips

Adin

Stabb

et al. 2011

Journal of Biological Chemistry

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Vibrio fischeri, a bioluminescent marine bacterium, exists in an exclusive symbiotic relationship with the Hawaiian bobtail squid, Euprymna scolopes, whose light organ it colonizes. Previously, it has been shown that the lipopolysaccharide (LPS) or free lipid A of V. fischeri can trigger morphological changes in the juvenile squid's light organ that occur upon colonization. To investigate the structural features that might be responsible for this phenomenon, the lipid A from V. fischeri ES114 LPS was isolated and characterized by multistage mass spectrometry (MS n ). A microheterogeneous mixture of mono-and diphosphorylated diglucosamine disaccharides was observed with variable states of acylation ranging from tetra-to octaacylated forms. All lipid A species, however, contained a set of conserved primary acyl chains consisting of an N- The bioluminescent bacterium Vibrio fischeri exists in a symbiotic relationship with the Hawaiian bobtail squid, Euprymna scolopes. Colonization of the juvenile squid's light organ by V. fischeri begins within hours of hatching (1). From the complex bacterial community present in seawater, V. fischeri, which represents less than 1% of the bacterial population, is exclusively recruited by E. scolopes in a multistep winnowing process (2). As the colonization of the juvenile's light organ progresses, a series of developmental changes occur in the tissues. The most dramatic of these morphogenetic events is the loss of a superficial ciliated field of cells important for the initial recruitment of V. fischeri. This process occurs over the ϳ96 -120 h following initial colonization by the symbiont (2) and does not occur without interactions with the symbiont in the deep crypt regions of the organ. Once the colonization is established, the squid continues to maintain a population of V. fischeri in its light organ, with cycles of daily flushing and repopulation by residual bacteria.The selection process that leads to the exclusive symbiotic relationship between V. fischeri and E. scolopes involves the interaction of bacterial surface components with host tissues. Previously, we showed that bacterial lipopolysaccharide (LPS) and lipid A can induce early stage apoptosis in the cells of the ciliated field of the juvenile squid's light organ (3). However, the effect was not species-specific, suggesting that a conserved portion of the lipid A may be the responsible component of the LPS structure (3). In later stages of the colonization process, bacterial peptidoglycan acts synergistically with LPS to induce most, if not all, of light organ morphogenesis (4).How the developmental signals of bacterial LPS and peptidoglycan, which are presented by the symbionts in the deep crypts of the light organ, are conveyed to the superficial tissue remains unknown, but one piece of the puzzle has recently been discovered. At hatching, the light organ has high levels of nitric oxide (NO). Following symbiont colonization of the crypts, the levels of both NO and the enzyme that catalyzes its production, nitric-o...

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The structure of the lipid anchor ofCampylobacter jejunipolysaccharide

Cited by 20 publications

References 32 publications

Conserved glycolipid termini in capsular polysaccharides synthesized by ATP-binding cassette transporter-dependent pathways in Gram-negative pathogens

Conserved glycolipid termini in capsular polysaccharides synthesized by ATP-binding cassette transporter-dependent pathways in Gram-negative pathogens

Campylobacter Polysaccharide Capsules: Virulence and Vaccines

The Lipid A from Vibrio fischeri Lipopolysaccharide

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