The complete structure of the core of the LPS from Plesiomonas shigelloides 302–73 and the identification of its O-antigen biological repeating unit

Pieretti, Giuseppina; Carillo, Sara; Lindner, Buko; Lanzetta, Rosa; Parrilli, Michelangelo; Jiménez, Natàlia; Regué, Miguel; Tomás, Juan M.; Corsaro, Maria Michela

doi:10.1016/j.carres.2010.09.007

Cited by 23 publications

(22 citation statements)

References 35 publications

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“…To date, LPS structures have been studied for 11 strains of P. shigelloides (Table 8) (156,157,158,159,160,161,162,163,164,165,166,167,168,169,170). The majority of LPS regions studied in the Enterobacteriaceae that link the core to the lipid A moiety (KdoI) contain at least one residue of 3-deoxy-D-manno-oct-2-(ketodeoxyoctonic) acid (KdoI) (156,159).…”

Section: Lipopolysaccharidementioning

confidence: 99%

“…This is based on the possession of the outer core disaccharide galactose A-glucosamine N and the substitution of ␤-glucose-HEPI, which is absent in the other major enteric LPS group, the Escherichia-Salmonella-Shigella LPS group (159). However, peculiar to P. shigelloides is the presence of ␤-galactose-HEPI as the substituted moiety instead of ␤-glucose-HEPI (157,158,159,172).…”

Section: Lipopolysaccharidementioning

confidence: 99%

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Plesiomonas shigelloides Revisited

Janda¹,

2016

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SUMMARYAfter many years in the familyVibrionaceae, the genusPlesiomonas, represented by a single species,P. shigelloides, currently resides in the familyEnterobacteriaceae, although its most appropriate phylogenetic position may yet to be determined. Common environmental reservoirs for plesiomonads include freshwater ecosystems and estuaries and inhabitants of these aquatic environs. Long suspected as being an etiologic agent of bacterial gastroenteritis, convincing evidence supporting this conclusion has accumulated over the past 2 decades in the form of a series of foodborne outbreaks solely or partially attributable toP. shigelloides. The prevalence ofP. shigelloidesenteritis varies considerably, with higher rates reported from Southeast Asia and Africa and lower numbers from North America and Europe. Reasons for these differences may include hygiene conditions, dietary habits, regional occupations, or other unknown factors. Other human illnesses caused byP. shigelloidesinclude septicemia and central nervous system disease, eye infections, and a variety of miscellaneous ailments. For years, recognizable virulence factors potentially associated withP. shigelloidespathogenicity were lacking; however, several good candidates now have been reported, including a cytotoxic hemolysin, iron acquisition systems, and lipopolysaccharide. WhileP. shigelloidesis easy to identify biochemically, it is often overlooked in stool samples due to its smaller colony size or relatively low prevalence in gastrointestinal samples. However, one FDA-approved PCR-based culture-independent diagnostic test system to detect multiple enteropathogens (FilmArray) includesP. shigelloideson its panel. Plesiomonads produce β-lactamases but are typically susceptible to many first-line antimicrobial agents, including quinolones and carbapenems.

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Section: Lipopolysaccharidementioning

confidence: 99%

Section: Lipopolysaccharidementioning

confidence: 99%

Plesiomonas shigelloides Revisited

Janda¹,

2016

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“…1). Also, purified LPS from both mutants 302-A and 302-B complemented with COS-PO1 and COS-PO2, respectively, showed the presence of deoxy sugars characteristics of O1-antigen LPS and all the monosaccharides from the LPS-core [17] (Fig. 2).…”

Section: Mutant Isolation and Analysesmentioning

confidence: 94%

“…1). Purified LPS from both mutants also showed a completely absence of deoxy sugars characteristics of O1-antigen LPS and the presence of all the monosaccharides from the LPS-core (Kdo, Hep, Gal, GalA, GlcN, [17]) (Fig. 2).…”

Section: Mutant Isolation and Analysesmentioning

confidence: 95%

“…So far, only two complete LPS molecules isolated from P. shigelloides CNCTC 113/92 (serotype O54) and CNCTC 144/92 (serotype O74) [14,15] were elucidated. Additionally the structures of the core oligosaccharide substituted with the O-specific chains from strain 302-73 (serotype O1) [16,17] and the O-specific polysaccharide from strain CNCTC 110/92 (serotype O51) [18] and AM36565 [19] were identified.…”

Section: Q1mentioning

confidence: 99%

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The Plesiomonas shigelloides wbO1 gene cluster and the role of O1-antigen LPS in pathogenicity

Aquilini

Merino

Tomás

2013

Microbial Pathogenesis

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Thank you for your assistance. HighlightsThe Plesiomonas shigelloides 302-73 strain (serotype O1) wb gene cluster. The cluster encodes 15 proteins in agreement with chemical structure. The mutants lacking this O1-antigen LPS unable to survive in serum or adhere. First report on genetics from a P. shigelloides O-antigen LPS not shared by Shigella. The Plesiomonas shigelloides 302-73 strain (serotype O1) wb gene cluster encodes 15 proteins which are consistent with the chemical structure of the O1-antigen lypopolysaccharide (LPS) previously described for this strain. The P. shigelloides O1-antigen LPS export uses the Wzy-dependent pathway as correspond to heteropolysaccharides structures. By the isolation of two mutants lacking this O1-antigen LPS, we could establish that the presence of the O1-antigen LPS is crucial for to survive in serum mainly to become resistant to complement. Also, it is an important factor in the bacterial adhesion and invasion to some eukaryotic cells, and in the ability to form biofilms. This is the first report on the genetics from a P. shigelloides O-antigen LPS cluster (wb) not shared by Shigella like P. shigelloides O17, the only one reported until now.

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Structural Analysis of the Core Oligosaccharide and the O‐Specific Polysaccharide from the Plesiomonas shigelloides O33:H3 (Strain CNCTC 34/89) Lipopolysaccharide

2013

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Lipopolysaccharides (LPS, endotoxin) with different core oligosaccharide glycoforms from the same species are common, but diversity among glycoforms reported to date has been related to terminal residues only. In this work, contrary to the variety of known LPS structures, we observed a 30 % replacement of glucosamine to glucose in the middle of the outer core region of the Plesiomonas shigelloides serotype O33:H3 (CNCTC 34/89) lipopolysaccharide. Such atypical modification within the same serotype raises questions about the biosynthesis of core structures. The core oligosaccharide was an undecasaccharide with a high level of O‐acetylation on the residue linked to the O‐specific polysaccharide. The core oligosaccharide, the O‐specific polysaccharide, and the linkage between them were determined by 1H and 13C NMR spectroscopy, mass spectrometry and chemical analysis. The presence of the O‐specific polysaccharide on the bacterial cell surface was confirmed by 1H high‐resolution magic angle spinning NMR spectroscopy.

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The complete structure of the core of the LPS from Plesiomonas shigelloides 302–73 and the identification of its O-antigen biological repeating unit

Cited by 23 publications

References 35 publications

Plesiomonas shigelloides Revisited

Plesiomonas shigelloides Revisited

The Plesiomonas shigelloides wbO1 gene cluster and the role of O1-antigen LPS in pathogenicity

Structural Analysis of the Core Oligosaccharide and the O‐Specific Polysaccharide from the Plesiomonas shigelloides O33:H3 (Strain CNCTC 34/89) Lipopolysaccharide

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