Cell-surface α-glucan in Campylobacter jejuni 81-176

Papp-Szabó, Erzsébet; Kanipes, Margaret I.; Guerry, Patricia; Monteiro, Mário A.

doi:10.1016/j.carres.2005.06.023

Cited by 21 publications

(20 citation statements)

References 13 publications

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“…The fragments corresponding to the main signals are identical to those of the spectrum previously published (Schmidt & Jann, 1982). More recently, PSs have been described in both C. jejuni NCTC 11168 and 81-176 (St Michael et al, 2002;Papp-Szabo et al, 2005) which have been deduced to be CPS in nature, although conclusive structural data describing the PS lipid anchor were not reported. Corcoran & Moran, 2005).…”

Section: Discussionsupporting

confidence: 74%

“…Subsequently, based on mutational analysis of the kpsM, kpsS and kpsC genes of C. jejuni, Karlyshev et al (2000) suggested that C. jejuni produces LOS, and not LPS, and that the previously described high-M r , LPS O-chains were capsular PS (CPS) in origin, and were serodominant. Although CPS and capsules have been deduced to be expressed in a number of C. jejuni strains (St Michael et al, 2002;Karlyshev et al, 2005;McNally et al, 2005;Papp-Szabo et al, 2005), a lipid anchor for the CPS has not been described. Confirming the independence of C. jejuni PS from LPS, studies by Oldfield et al (2002) with NCTC 11828 (HS:6) showed that when the waaF gene, a heptosyltransferase II enzyme involved in LPS core biosynthesis, was deleted, the electrophoretic mobility of high-M r antigenic PS was unaffected.…”

Section: Introductionmentioning

confidence: 99%

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The structure of the lipid anchor ofCampylobacter jejunipolysaccharide

Corcoran

Annuk

Moran

2006

FEMS Microbiology Letters

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Campylobacter jejuni is a leading cause of gastroenteritis in humans. Campylobacter jejuni produces extracellular polysaccharides that have been characterized structurally and shown to be independent of lipopolysaccharides. Furthermore, it has been suggested that these C. jejuni polysaccharides are capsular in nature, although their lipid anchor has not been identified. In this report, the occurrence of a lipid-linked capsular-like polysaccharide in C. jejuni is conclusively shown, and the lipid anchor identified as dipalmitoyl-glycerophosphate.

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Section: Discussionsupporting

confidence: 74%

Section: Introductionmentioning

confidence: 99%

The structure of the lipid anchor ofCampylobacter jejunipolysaccharide

Corcoran

Annuk

Moran

2006

FEMS Microbiology Letters

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“…Consistent with the results of this study with C. jejuni NCTC 11168 showing the occurrence of a third PRC, preliminary observations of a Calcofluor White‐reactive moiety, independent of capsular polysaccharide, have been reported in C. jejuni 81–176 (McLennan et al , 2005). Nevertheless, in C. jejuni 81–176, in addition to lipooligosaccharide and serodominant capsular polysaccharide, Papp‐Szabo et al (2005) have described a cell surface α‐(1,4)‐glucan that was inferred to be a second capsular polysaccharide, but data concerning the capsular lipid anchor were not provided.…”

Section: Discussionmentioning

confidence: 99%

Influence of growth conditions on diverse polysaccharide production byCampylobacter jejuni

Corcoran

Moran

2007

FEMS Immunol Med Microbiol

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Campylobacter jejuni is the leading bacterial cause of gastroenteritis worldwide. The present study was undertaken to determine the forms of polysaccharide-related compounds (PRCs) produced by C. jejuni and the culture conditions influencing their production. Expression of polysaccharides by C. jejuni was influenced by culture medium composition and growth phase. In addition to the production of lipooligosaccharide and capsular polysaccharide, a previously undescribed polysaccharide, not related to capsular polysaccharide, was shown to occur in C. jejuni in batch liquid and chemostat cultures. Thus, a variety of PRCs are produced by C. jejuni, and this should be considered when growing the bacterium in vitro for pathogenesis studies.

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“…These observations suggest cell envelope perturbations despite the fact that we were unable to detect overt changes in outer membrane protein profiles or cell surface hydrophobicity. One potential explanation for the latter is that C. jejuni 81-176 harbors an extensive CPS, including an additional ␣-glucan capsule (70), that may interfere with detection of hydrophobicity alterations associated with LOS truncations. Nonetheless, consistent with envelope perturbations, our LOS mutants exhibited SDS sensitivities similar to those reported for the ⌬waaF mutant and the large LOS deletion mutants of strain 11168 (37,56), and our AMP observations are consistent with a recent E. coli study hypothesizing that negative cell surface charges normally buried by the LPS/LOS are exposed in LPS/LOS mutants and thereby more available to interact with cationic molecules (5).…”

Section: Vol 192 2010 C Jejuni Los Core Residues In Pathogenesis 2189mentioning

confidence: 99%

Effects of SequentialCampylobacter jejuni81-176 Lipooligosaccharide Core Truncations on Biofilm Formation, Stress Survival, and Pathogenesis

et al. 2010

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Campylobacter jejuni is a highly prevalent human pathogen for which pathogenic and stress survival strategies remain relatively poorly understood. We previously found that a C. jejuni strain 81-176 mutant defective for key virulence and stress survival attributes was also hyper-biofilm and hyperreactive to the UV fluorescent dye calcofluor white (CFW). We hypothesized that screening for CFW hyperreactive mutants would identify additional genes required for C. jejuni pathogenesis properties. Surprisingly, two such mutants harbored lesions in lipooligosaccharide (LOS) genes (waaF and lgtF), indicating a complete loss of the LOS outer core region. We utilized this as an opportunity to explore the role of each LOS core-specific moiety in the pathogenesis and stress survival of this strain and thus also constructed ⌬galT and ⌬cstII mutants with more minor LOS truncations. Interestingly, we found that mutants lacking the LOS outer core (⌬waaF and ⌬lgtF but not ⌬galT or ⌬cstII mutants) exhibited enhanced biofilm formation. The presence of the complete outer core was also necessary for resistance to complement-mediated killing. In contrast, any LOS truncation, even that of the terminal sialic acid (⌬cstII), resulted in diminished resistance to polymyxin B. The cathelicidin LL-37 was found to be active against C. jejuni, with the LOS mutants exhibiting modest but tiled alterations in LL-37 sensitivity. The ⌬waaF mutant but not the other LOS mutant strains also exhibited a defect in intraepithelial cell survival, an aspect of C. jejuni pathogenesis that has only recently begun to be clarified. Finally, using a mouse competition model, we now provide the first direct evidence for the importance of the C. jejuni LOS in host colonization. Collectively, this study has uncovered novel roles for the C. jejuni LOS, highlights the dynamic nature of the C. jejuni cell envelope, and provides insight into the contribution of specific LOS core moieties to stress survival and pathogenesis.

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Cell-surface α-glucan in Campylobacter jejuni 81-176

Cited by 21 publications

References 13 publications

The structure of the lipid anchor ofCampylobacter jejunipolysaccharide

The structure of the lipid anchor ofCampylobacter jejunipolysaccharide

Influence of growth conditions on diverse polysaccharide production byCampylobacter jejuni

Effects of SequentialCampylobacter jejuni81-176 Lipooligosaccharide Core Truncations on Biofilm Formation, Stress Survival, and Pathogenesis

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