Analysis of the capsular polysaccharide biosynthesis locus of <i>Porphyromonas gingivalis</i> and development of a K1‐specific polymerase chain reaction‐based serotyping assay

Brunner, Jorg; Winkelhoff, van Arie

doi:10.1111/j.1600-0765.2007.01075.x

Cited by 10 publications

(12 citation statements)

References 29 publications

(42 reference statements)

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“…PG0117 and PG0118 are called absent in each test strain as concluded from our hybridization experiments. This supports the choice of these genes to design a K1-specific PCR for serotyping in our group [54]. All test strains are found to be aberrant for at least 8 genes, except strain 34-4 (K7) which only shows aberrance in 5 genes.…”

Section: Resultssupporting

confidence: 64%

The core genome of the anaerobic oral pathogenic bacterium Porphyromonas gingivalis

et al. 2010

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BackgroundThe Gram negative anaerobic bacterium Porphyromonas gingivalis has long been recognized as a causative agent of periodontitis. Periodontitis is a chronic infectious disease of the tooth supporting tissues eventually leading to tooth-loss. Capsular polysaccharide (CPS) of P. gingivalis has been shown to be an important virulence determinant. Seven capsular serotypes have been described. Here, we used micro-array based comparative genomic hybridization analysis (CGH) to analyze a representative of each of the capsular serotypes and a non-encapsulated strain against the highly virulent and sequenced W83 strain. We defined absent calls using Arabidopsis thaliana negative control probes, with the aim to distinguish between aberrations due to mutations and gene gain/loss.ResultsOur analyses allowed us to call aberrant genes, absent genes and divergent regions in each of the test strains. A conserved core P. gingivalis genome was described, which consists of 80% of the analyzed genes from the sequenced W83 strain. The percentage of aberrant genes between the test strains and control strain W83 was 8.2% to 13.7%. Among the aberrant genes many CPS biosynthesis genes were found. Most other virulence related genes could be found in the conserved core genome. Comparing highly virulent strains with less virulent strains indicates that hmuS, a putative CobN/Mg chelatase involved in heme uptake, may be a more relevant virulence determinant than previously expected. Furthermore, the description of the 39 W83-specific genes could give more insight in why this strain is more virulent than others.ConclusionAnalyses of the genetic content of the P. gingivalis capsular serotypes allowed the description of a P. gingivalis core genome. The high resolution data from three types of analysis of triplicate hybridization experiments may explain the higher divergence between P. gingivalis strains than previously recognized.

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Section: Resultssupporting

confidence: 64%

The core genome of the anaerobic oral pathogenic bacterium Porphyromonas gingivalis

et al. 2010

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“…The majority of P. gingivalis isolates are encapsulated. Based on the serotypes of K antigens, P. gingivalis isolates can be divided into at least six groups (K1 to K6) (7,34), highlighting the complexity of carbohydrates presented in P. gingivalis capsular polysaccharides. Little is known about the structure and composition of carbohydrates in the capsule of P. gingivalis.…”

Section: Discussionmentioning

confidence: 99%

Abrogation of Neuraminidase Reduces Biofilm Formation, Capsule Biosynthesis, and Virulence of Porphyromonas gingivalis

Kurniyati

Hu³

et al. 2012

Infect Immun

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The oral bacterium Porphyromonas gingivalis is a key etiological agent of human periodontitis, a prevalent chronic disease that affects up to 80% of the adult population worldwide. P. gingivalis exhibits neuraminidase activity. However, the enzyme responsible for this activity, its biochemical features, and its role in the physiology and virulence of P. gingivalis remain elusive. In this report, we found that P. gingivalis encodes a neuraminidase, PG0352 (Sia Pg ). Transcriptional analysis showed that PG0352 is monocistronic and is regulated by a sigma 70 -like promoter. Biochemical analyses demonstrated that Sia Pg is an exo-␣-neuraminidase that cleaves glycosidic-linked sialic acids. Cryoelectron microscopy and tomography analyses revealed that the PG0352 deletion mutant (⌬PG352) failed to produce an intact capsule layer. Compared to the wild type, in vitro studies showed that ⌬PG352 formed less biofilm and was less resistant to killing by the host complement. In vivo studies showed that while the wild type caused a spreading type of infection that affected multiple organs and all infected mice were killed, ⌬PG352 only caused localized infection and all animals survived. Taken together, these results demonstrate that Sia Pg is an important virulence factor that contributes to the biofilm formation, capsule biosynthesis, and pathogenicity of P. gingivalis, and it can potentially serve as a new target for developing therapeutic agents against P. gingivalis infection.

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“…It is well known that differences in P. gingivalis capsular (K) and FIMA antigens may influence virulence [8,9,27,32,42]. However, our choice for microscopic detection of capsule and fimbriae instead of immune detection of their antigens was due to the large variability of the capsular and major fimbriae antigens within P. gingivalis, requiring the use of several non commercially available sera, plus the existence of still not typable strains based on the K or FIMA antigens.…”

Section: Discussionmentioning

confidence: 98%

“…Furthermore, capsule production by certain P. gingivalis strains was associated with increased virulence [21,27], properties such as resistance against desiccation, osmotic stress, oxygen toxicity and phagocytic engulfment [11], induction of a lower host response [9,37], and biofilm formation [13]. The capsular polysaccharide locus shows evidence of being acquired by horizontal transfer [1,10], and is very polymorphic, leading to seven capsule known antigens [8] and non typable strains [26]. Although a gene encoding a glycosiltransferase (pg0106) was shown to be essential for capsule production [13], it is present in most P. gingivalis isolates independently on the capsule expression [10].…”

Section: Introductionmentioning

confidence: 99%

Lineage variability in surface components expression within Porphyromonas gingivalis

Teixeira

D'Epiro

Pinheiro

et al. 2014

Microbial Pathogenesis

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Analysis of the capsular polysaccharide biosynthesis locus of Porphyromonas gingivalis and development of a K1‐specific polymerase chain reaction‐based serotyping assay

Cited by 10 publications

References 29 publications

The core genome of the anaerobic oral pathogenic bacterium Porphyromonas gingivalis

The core genome of the anaerobic oral pathogenic bacterium Porphyromonas gingivalis

Abrogation of Neuraminidase Reduces Biofilm Formation, Capsule Biosynthesis, and Virulence of Porphyromonas gingivalis

Lineage variability in surface components expression within Porphyromonas gingivalis

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