Structural and Biological Characterization of a Capsular Polysaccharide Produced by Staphylococcus haemolyticus

Channing Laboratory, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.
Journal of bacteriology (Impact Factor: 2.81). 03/2008; 190(5):1649-57. DOI: 10.1128/JB.01648-07
Source: PubMed


The DNA sequence of the genome of Staphylococcus haemolyticus JCSC1435 revealed a putative capsule operon composed of 13 genes in tandem. The first seven genes (capABCDEFGSh) showed ≥57% similarity with the Staphylococcus aureus cap5 or cap8 locus. However, the capHIJKLMSh genes are unique to S. haemolyticus and include genes encoding a putative flippase, an aminotransferase, two glycosyltransferases, and a transcriptional regulator.
Capsule-like material was readily apparent by immunoelectron microscopy on bacteria harvested in the postexponential phase
of growth. Electron micrographs of a JCSC1435 mutant with a deleted cap region lacked the capsule-like material. Both strains produced small amounts of surface-associated material that reacted
with antibodies to polyglutamic acid. S. haemolyticus cap genes were amplified from four of seven clinical isolates of S. haemolyticus from humans, and three of these strains produced a serologically cross-reactive capsular polysaccharide. In vitro assays
demonstrated that the acapsular mutant strain showed greater biofilm formation but was more susceptible to complement-mediated
opsonophagocytic killing than the parent strain. Structural characterization of capsule purified from S. haemolyticus strain JCSC1435 showed a trisaccharide repeating unit: −3-α-l-FucNAc-3-(2-NAc-4-N-Asp-2,4,6-trideoxy-β-d-Glc)-4-α-d-GlcNAc-. This structure is unique among staphylococcal polysaccharides in that its composition includes a trideoxy sugar
residue with aspartic acid as an N-acyl substituent.

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Available from: Evgeny Vinogradov, Jan 30, 2014
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    • "Campylobacter jejuni 47 Polysaccharide [18] [19] Escherichia coli 80 Polysaccharide [20] Haemophilus influenzae 6 Polysaccharide [21] Klebsiella pneumoniae 82 Polysaccharide [22] Neisseria meningitidis 13 Polysaccharide [23] Pasteurella multocida 4 Polysaccharide [24] Pseudomonas aeruginosa 1 Polysaccharide [25] Salmonella enterica serovar Typhi 1 Polysaccharide [26] Streptococcus pneumoniae 94 Polysaccharide [27] [28] Streptococcus agalactiae 9 Polysaccharide [29] Streptococcus pyogenes 1 Polysaccharide [30] Streptococcus suis 35 Polysaccharide [31] Staphylococcus aureus 11 Polysaccharide [32] Staphylococcus haemolyticus 1 Polysaccharide [33] Bacillus anthracis 1 Polyglutamate [34] "

    Full-text · Chapter · Dec 2015
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    • "These properties of polysaccharides pave the way for numerous applications aimed at prevention of detrimental biofilms (Rendueles et al., 2013). Self-inhibition by extracellular polysaccharides was demonstrated for E. coli and K. kingae; however, in many other cases of biofilm inhibition of competitor species by exopolysaccharides, the inhibitory effect on the producing bacterium was not examined (Joseph and Wright, 2004; Davey and Duncan, 2006; Honma et al., 2007; Flahaut et al., 2008; Kouzuma et al., 2010). Given the nonspecific inhibitory effect of extracellular polysaccharides, which results from alteration of the surface physicochemical properties, it is conceivable that biofilm limitation by the producing bacterium occurs widely. "
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    ABSTRACT: The transition between planktonic growth and biofilm formation represents a tightly regulated developmental shift that has substantial impact on cell fate. Here, we highlight different mechanisms through which bacteria limit their own biofilm development. The mechanisms involved in these self-inhibition processes include: (i) regulation by secreted small molecules, which govern intricate signaling cascades that eventually decrease biofilm development, (ii) extracellular polysaccharides capable of modifying the physicochemical properties of the substratum, and (iii) extracellular DNA that masks an adhesive structure. These mechanisms, which rely on substances produced by the bacterium and released into the extracellular milieu, suggest regulation at the communal level. In addition, we provide specific examples of environmental cues (e.g. blue-light or glucose level) that trigger a cellular response reducing biofilm development. All together, we describe a diverse array of mechanisms underlying self-inhibition of biofilm development in different bacteria, and discuss possible advantages of these processes.
    Full-text · Article · Aug 2014 · Environmental Microbiology
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    • "It is well known that bacterial exopolysaccharides exhibit highly variable structures and it is likely that they also perform additional functions besides their implied function in matrix stabilization and energy storage (Rendueles et al., 2013). In fact, several studies showed that certain bacterial mutants deficient in capsular polysaccharide production exhibit increased biofilm formation (Valle et al., 2006; Flahaut et al., 2008). These observations suggest that some bacterial exopolysaccharides can perform functions that inhibit or destabilize the biofilm. "
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    ABSTRACT: Considering the increasing impact of bacterial biofilms on human health, industrial and food-processing activities, the interest in the development of new approaches for the prevention and treatment of adhesion and biofilm formation capabilities has increased. A viable approach should target adhesive properties without affecting bacterial vitality in order to avoid the rapid appearance of escape mutants. It is known that marine bacteria belonging to the genus Pseudoalteromonas produce compounds of biotechnological interest, including anti-biofilm molecules. Pseudoalteromonas haloplanktis TAC125 is the first Antarctic Gram-negative strain whose genome was sequenced. In this work the anti-biofilm activity of P. haloplanktis supernatant was examined on different staphylococci. Results obtained demonstrated that supernatant of P. haloplanktis, grown in static condition, inhibits biofilm of Staphylococcus epidermidis. In order to define the chemical nature of the biofilm-inhibiting compound, the supernatant was subject to various treatments. Data reported demonstrated that the biologically active component is sensible to treatment with sodium periodate suggesting its saccharidic nature.
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