Structure of the O polysaccharides and serological classification of <i>Pseudomonas syringae</i> pv. porri from genomospecies 4

Zdorovenko, Evelina L.; Zatonskii, George V.; Kocharova, Nina A.; Shashkov, A. S.; Knirel, Yuriy A.; Ovod, Vladimir

doi:10.1046/j.1432-1033.2003.03354.x

Cited by 12 publications

(5 citation statements)

References 29 publications

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“…In Gram-negative bacteria, part of the products produced during this metabolism, especially rhamnose sugars in Pspo, are shuttled towards the production of lipopolysaccharides (LPS). Indeed, the Pspo O-antigen consists of L-rhamnose repeats [22]. LPS form a significant part of the outer membrane of Gram-negative bacteria and have previously been described to be recognized by certain phages as phage receptors [16].…”

Section: Elucidation Of the Differences In Bacterial Receptors For Phmentioning

confidence: 99%

Preparing for the KIL: Receptor Analysis of Pseudomonas syringae pv. porri Phages and Their Impact on Bacterial Virulence

Holtappels

Kerremans

Busschots

et al. 2020

IJMS

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The prevalence of Pseudomonas syringae pv. porri (Pspo) in Belgium continues to increase and sustainable treatments for this pathogen remain unavailable. A potentially attractive biocontrol strategy would be the application of bacteriophages. The ideal application strategy of phages in an agricultural setting remains unclear, especially in a field-based production such as for leek plants in Flanders. Therefore, more insight in bacteria–phage interaction is required, along with the evaluation of different application strategies. In this study, we further characterized the infection strategy of two Pspo phages, KIL3b and KIL5. We found that both phages recognize lipopolysaccharide (LPS) moieties on the surface of the bacterium. LPS is an important pathogenicity factor of Pspo. Our data also suggest that KIL5 requires an additional protein in the bacterial cytoplasmatic membrane to efficiently infect its host. Virulence tests showed that this protein also contributes to Pspo virulence. Furthermore, a cocktail of both phages was applied in a seed bioassay. A combination of KIL3b and KIL5 reduced the bacterial concentration 100-fold. However, in vitro Pspo resistance against phage infection developed quite rapidly. However, the impact of this phage resistance might be mitigated as is suggested by the fact that those resistance mutations preferably occur in genes involved in LPS metabolism, and that the virulence of those mutants is possibly reduced. Our data suggest that the phage cocktail has promising potential to lower the prevalence of Pspo and to be integrated in a pest management strategy. Targeted research is needed to further explore the applicability of the phages in combination with other disease control strategies.

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Section: Elucidation Of the Differences In Bacterial Receptors For Phmentioning

confidence: 99%

Preparing for the KIL: Receptor Analysis of Pseudomonas syringae pv. porri Phages and Their Impact on Bacterial Virulence

Holtappels

Kerremans

Busschots

et al. 2020

IJMS

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“…LPS is composed of lipid A, a core oligosaccharide, and an O‐polysaccharide (O‐antigen) built up of oligosaccharide repeats. The structures of the O‐polysaccharides of all known serologically distinguishable smooth strains of P. syringae have been determined [3–12]. Aiming at solving the problems of recognition, taxonomy and classification of P. syringae strains, we established, for the first time, the full structure of the core region of the LPS from a rough strain of P. syringae pv.…”

mentioning

confidence: 99%

Structure of the core oligosaccharide of a rough‐type lipopolysaccharide of Pseudomonas syringae pv. phaseolicola

Zdorovenko

Vinogradov

Zdorovenko

et al. 2004

European Journal of Biochemistry

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The core structure of the lipopolysaccharide (LPS) isolated from a rough strain of the phytopathogenic bacterium Pseudomonas syringae pv. phaseolicola, GSPB 711, was investigated by sugar and methylation analyses, Fourier transform ion‐cyclotron resonance ESI MS, and one‐ and two‐dimensional 1H‐, 13C‐ and 31P‐NMR spectroscopy. Strong alkaline deacylation of the LPS resulted in two core‐lipid A backbone undecasaccharide pentakisphosphates in the ratio ≈ 2.5 : 1, which corresponded to outer core glycoforms 1 and 2 terminated with either l‐rhamnose or 3‐deoxy‐d‐manno‐oct‐2‐ulosonic acid (Kdo), respectively. Mild acid degradation of the LPS gave the major glycoform 1 core octasaccharide and a minor truncated glycoform 2 core heptasaccharide, which resulted from the cleavage of the terminal Kdo residues. The inner core of P. syringae is distinguished by a high degree of phosphorylation of l‐glycero‐d‐manno‐heptose residues with phosphate, diphosphate and ethanolamine diphosphate groups. The glycoform 1 core is structurally similar but not identical to one of the core glycoforms of the human pathogenic bacterium Pseudomonas aeruginosa. The outer core composition and structure may be useful as a chemotaxonomic marker for the P. syringae group of bacteria, whereas a more conserved inner core structure appears to be representative for the whole genus Pseudomonas.

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“…It is released with vesicle-containing enzymes and outer membrane (OM). Its extended formula was determined in 2003 (Figure 1); it is anchored to the OM through the lipid A which binds to the 3-deoxy-d-manno-2-octulosonic acid (KDO), the first glycoside of the core oligosaccharide, bound to the distal O antigen, a highly variable region [77,78]. A metabolic crossroad between the LPS and alginate biosynthesis (Figure 2) is mannose-6-phosphate isomerization to mannose-1-phosphate by phosphomannomutase (Alg C).…”

Section: Pseudomonas Aeruginosa -An Armory Withinmentioning

confidence: 99%

Host-Pathogen Interaction in the Lung of Patients Infected withPseudomonas aeruginosa

Grumelli¹

2019

Pseudomonas Aeruginosa - An Armory Within

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Pseudomonas aeruginosa is an opportunistic bacterium that can proliferate in the soil, water, and even humans if they are immunologically depressed. During lung infections, P. aeruginosa goes through significant morphological changes turning into the mucoid form after which its eradication becomes almost impossible. Within this chapter, we explore the bioenergetics changes produced within P. aeruginosa during infections in humans and the metabolic pathways that are involved in those changes that lead to chronic infection. 2 transmembrane conductance regulator (CFTR) identified as F508, G542X, G551D, W1282X, R1162X, and N1303K [24, 25]. CF also has co-morbidity such as liver cirrhosis [26] with 18% prevalence [27,28] of P. aeruginosa infection in this subset. Host-bacteria interaction in acute infection Lung changes upon bacterial invasionThe flagella and lipopolysaccharide (LPS) from P. aeruginosa are the first to contact the ciliated epithelial cells [29]. In the airways, these cells are covered by the surfactants containing 45% less NaCl and 600 more K + than in plasma [30], while the alveolar epithelial cells are covered by a surfactant layer that contains mostly phosphatidylcholine (80%) [31] and surfactant proteins A, B, C, and D [32, 33] that bind LPS in a calcium-dependent manner [34]. After the surfactant layer is crossed, the flagellum binds to the epithelial cells through toll-like receptors (TLR) 2, 3, 4 and 5 [35][36][37][38][39][40] that are quickly endocytosed to be degraded in the proteasome. The activated TLR5 induces the macrophages chemoattractants CXCL1, CXCL2, and neutrophil chemokine CCL20, which are inhibited by TLR5 inhibitors [41]. The peptides digested are then presented to macrophages and dendritic cells.When LPS binds to the host cells, where CFTR is also a receptor [42], it upregulates NF-κB at the gene level (Table 1), promoting inflammation [43] by secretion of IL1, IL6, IL8, ICAM-1, and also CXCL1 [44][45][46][47], although in different degrees of regulation. For example, CXCL1 expression is orchestrated by a fatty acid-binding protein (FABP4) that delivers fatty acids from the cytoplasm to the nuclear receptor PPAR. These prompt macrophage signaling through the myeloid differentiation protein-88 (MyD88) to induce cytokine production following engagement of TLRs with LPS [48-51]. Macrophages require MyD88 to produce CXCL1 but also eicosapentaenoic acid and docosahexaenoic acid, both substrates of FABP4. This demonstrates the importance of fatty acid metabolism to promote host resistance to P. aeruginosa, facilitating macrophage-neutrophil cross-talk during the infection [52,53].The T cells also play an important role in acute infection. IL17 producing T cells are expanded [54], via expression of STAT3 and retinoid orphan receptor [55]; these steps are crucial for B cell activation and immunoglobulin release for bacterial clearance [56]. On the contrary, excess of T regulatory cells (Treg) are associated with secondary P. aeruginosa infections, because depletion of Tregs decreases ...

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Structure of the O polysaccharides and serological classification of Pseudomonas syringae pv. porri from genomospecies 4

Cited by 12 publications

References 29 publications

Preparing for the KIL: Receptor Analysis of Pseudomonas syringae pv. porri Phages and Their Impact on Bacterial Virulence

Preparing for the KIL: Receptor Analysis of Pseudomonas syringae pv. porri Phages and Their Impact on Bacterial Virulence

Structure of the core oligosaccharide of a rough‐type lipopolysaccharide of Pseudomonas syringae pv. phaseolicola

Host-Pathogen Interaction in the Lung of Patients Infected withPseudomonas aeruginosa

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