Alginate acetylation influences initial surface colonization by mucoid Pseudomonas aeruginosa

Tielen, Petra; Strathmann, Martin; Jaeger, Karl‐Erich; Flemming, Hans‐Curt; Wingender, Jost

doi:10.1016/j.micres.2004.11.003

Cited by 98 publications

(73 citation statements)

References 38 publications

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“…A mutation in algJ synthesizes alginate lacking O-acetyl groups, and this strain is significantly impaired in surface attachment and biofilm development (48). A separate study demonstrated that alginate acetylation was necessary for the aggregation of bacteria into microcolonies (68). Thus, it appears that acetyl groups help mediate interactions between neighboring cells and surface colonization, and these factors are important in the ability of strains to form robust biofilms.…”

Section: Figmentioning

confidence: 99%

PelA Deacetylase Activity Is Required for Pel Polysaccharide Synthesis in Pseudomonas aeruginosa

et al. 2013

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The Pel polysaccharide serves as an intercellular adhesin for the formation and maintenance of biofilms in the opportunistic pathogen Pseudomonas aeruginosa. Pel biosynthesis requires the products of a seven-gene operon, pelA-pelG, all of which are necessary for Pel-dependent biofilm formation and Pel-related phenotypes. One of the genes, pelA, encodes a protein with a predicted polysaccharide deacetylase domain. In this work, the role of the putative deacetylase domain in Pel production was examined. We first established that purified recombinant PelA hydrolyzed the pseudosubstrate p-nitrophenyl acetate in vitro, and site-specific mutations of predicted deacetylase active-site residues reduced activity greater than 10-fold. Additionally, these mutants were deficient in Pel-dependent biofilm formation and wrinkly colony morphology in vivo. Subcellular fractionation experiments demonstrate that PelA localizes to both the membrane and periplasmic fractions. Finally, antiserum against the Pel polysaccharide was generated, and PelA deacetylase mutants do not produce Pel-reactive material. Taken together, these results suggest that the deacetylase activity of PelA is important for the production of the Pel polysaccharide.

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Section: Figmentioning

confidence: 99%

PelA Deacetylase Activity Is Required for Pel Polysaccharide Synthesis in Pseudomonas aeruginosa

et al. 2013

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“…Results from several independent laboratories have shown that overproduction of acetylated alginate leads to significant architectural and morphological changes in the biofilm [10][11][12][13]. This translates into increased resistance to antimicrobials [10] or IFN-gamma-mediated killing by cells of the innate immune system [14].…”

Section: Alginatementioning

confidence: 99%

Role of polysaccharides in Pseudomonas aeruginosa biofilm development

Ryder

Byrd

Wozniak

2007

Current Opinion in Microbiology

508

385

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During the past decade, there has been a renewed interest in using P. aeruginosa as a model system for biofilm development and pathogenesis. Since the biofilm matrix represents a critical interface between the bacterium and the host or its environment, considerable effort has been expended to acquire a more complete understanding of the matrix composition. Here, we focus on recent developments regarding the roles of alginate, Psl, and Pel polysaccharides in the biofilm matrix.

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“…In many bacteria, O-acetylation alters the physicochemical properties of capsule by changing the conformation of capsular repeat units (13) or increasing viscosity (14). O-acetylation also alters the host-pathogen interaction by creating immunogenic epitopes (11,13,15), by neutralizing reactive chlorine species (16,17), and/or by mediating resistance to lysozyme and complement deposition (18)(19)(20)(21).…”

mentioning

confidence: 99%

The Pneumococcal Serotype 15C Capsule Is Partially O-Acetylated and Allows for Limited Evasion of 23-Valent Pneumococcal Polysaccharide Vaccine-Elicited Anti-Serotype 15B Antibodies

Spencer

Shenoy

Orihuela

et al. 2017

Clin Vaccine Immunol

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As a species, Streptococcus pneumoniae (the pneumococcus) utilizes a diverse array of capsular polysaccharides to evade the host. In contrast to large variations in sugar composition and linkage formation, O-acetylation is a subtle capsular modification that nonetheless has a large impact on capsular shielding and recognition of the capsule by vaccine-elicited antibodies. Serotype 15B, which is included in the 23-valent pneumococcal polysaccharide vaccine (PPV23), carries the putative O-acetyltransferase gene wciZ. The coding sequence of wciZ contains eight consecutive TA repeats [(TA) 8 ]. Replication slippage is thought to result in the addition or loss of TA repeats, subsequently causing frameshift and truncation of WciZ to yield a nonacetylated serotype, 15C. Using sensitive serological tools, we show that serotype 15C isolates whose wciZ contains seven or nine TA repeats retain partial O-acetylation, while serotype 15C isolates whose wciZ contains six TA repeats have barely detectable O-acetylation. We confirmed by inhibition enzyme-linked immunosorbent assay that (TA) 7 serotype 15C is ϳ0.1% as acetylated as serotype 15B, while serotype 15X is nonacetylated. To eliminate the impact of genetic background, we created isogenic serotype 15B, (TA) 7 serotype 15C, and 15BΔwciZ (15X) strains and found that reduction or absence of WciZ-mediated O-acetylation did not affect capsular shielding from phagocytes, biofilm formation, adhesion to nasopharyngeal cells, desiccation tolerance, or murine colonization. Sera from PPV23-immunized persons opsonized serotype 15B significantly but only slightly better than serotypes 15C and 15X; thus, PPV23 may not result in expansion of serotype 15C.KEYWORDS O-acetyltransferase, O-acetylation, capsule diversity, pneumococcal vaccine, capsular polysaccharide, serotyping, replication slippage S treptococcus pneumoniae (the pneumococcus), a Gram-positive human pathogen, mediates pneumonia and invasive diseases such as septicemia and meningitis and colonizes 6 to 76% of the world's pediatric population (1-3). Pneumococcal diseases are the leading cause of death in children under 5 years old (4), and pneumococcal capsular polysaccharide is the organism's most significant virulence factor as it shields the pneumococcus from various chemical and immune assaults (5). As a result, nonencapsulated pneumococci rarely cause pneumonia or invasive pneumococcal disease (6-8). Pneumococcal capsular types differ in their shielding abilities; therefore, some capsule types are more virulent than others (9, 10). Our previous studies have indicated that small chemical modifications of the capsular repeat unit result in differential shielding of closely related serotypes (11,12).An important capsular modification is O-acetylation: an uncharged, but polar, acetyl

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Alginate acetylation influences initial surface colonization by mucoid Pseudomonas aeruginosa

Cited by 98 publications

References 38 publications

PelA Deacetylase Activity Is Required for Pel Polysaccharide Synthesis in Pseudomonas aeruginosa

PelA Deacetylase Activity Is Required for Pel Polysaccharide Synthesis in Pseudomonas aeruginosa

Role of polysaccharides in Pseudomonas aeruginosa biofilm development

The Pneumococcal Serotype 15C Capsule Is Partially O-Acetylated and Allows for Limited Evasion of 23-Valent Pneumococcal Polysaccharide Vaccine-Elicited Anti-Serotype 15B Antibodies

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