Adhesion of <i>Porphyromonas gingivalis</i>. Serotypes to Pocket Epithelium

Dierickx, Kurt; Pauwels, Martine; Laine, Marja L.; Eldere, Johan Van; Cassiman, Jean Jacques; Winkelhoff, A.J. van; Steenberghe, Daniël van; Quirynen, Marc

doi:10.1902/jop.2003.74.6.844

Cited by 33 publications

(38 citation statements)

References 24 publications

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“…This assay was previously used to assess the hydrophobicity of P. gingivalis strains. It was shown that strains ATCC 33277 and 381 are hydrophobic and do not make significant amounts of capsular polysaccharide (16,82), and indeed, we found that these strains partitioned into hexadecane by approximately 90%. Increased partitioning was not observed in the respective PG0106 mutants.…”

Section: Isolation Of the Pg0106 Mutantsupporting

confidence: 67%

“…6B). As noted above, it has been shown that strains ATCC 33277 and 381 are hydro- phobic and do not make significant amounts of capsular polysaccharide (16,82). India ink staining of these two strains is shown in Fig.…”

Section: Isolation Of the Pg0106 Mutantmentioning

confidence: 74%

“…Like that in many encapsulated pathogenic bacteria, capsule expression in P. gingivalis is linked to pathogenicity. Interestingly, strains that produce a capsule have been shown to cause a spreading type of infection in mice, with recovery of the organism from blood, spleen, and kidneys (16,52), while infections with strains that do not synthesize capsule (strains 381 and 33277) typically attach and result in localized abscesses (43,52), suggesting that encapsulation is linked to dissemination and not attachment. Our results show that capsule expression in P. gingivalis blocks biofilm formation and hence could enhance dissemination.…”

Section: Discussionmentioning

confidence: 99%

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Enhanced Biofilm Formation and Loss of Capsule Synthesis: Deletion of a Putative Glycosyltransferase inPorphyromonas gingivalis

Davey¹,

Duncan²

2006

J Bacteriol

112

104

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Periodontitis is a biofilm-mediated disease. Porphyromonas gingivalis is an obligate anaerobe consistently associated with severe manifestations of this disease. As an opportunistic pathogen, the ability to proliferate within and disseminate from subgingival biofilm (plaque) is central to its virulence. Here, we report the isolation of a P. gingivalis transposon insertion mutant altered in biofilm development and the reconstruction and characterization of this mutation in three different wild-type strains. The mutation responsible for the altered biofilm phenotype was in a gene with high sequence similarity (ϳ61%) to a glycosyltransferase gene. The gene is located in a region of the chromosome that includes up to 16 genes predicted to be involved in the synthesis and transport of capsular polysaccharide. The phenotype of the reconstructed mutation in all three wild-type backgrounds is that of enhanced biofilm formation. In addition, in strain W83, a strain that is encapsulated, the glycosyltransferase mutation resulted in a loss of capsule. Further experiments showed that the W83 mutant strain was more hydrophobic and exhibited increased autoaggregation. Our results indicate that we have identified a gene involved in capsularpolysaccharide synthesis in P. gingivalis and that the production of capsule prevented attachment and the initiation of in vitro biofilm formation on polystyrene microtiter plates.The clinical importance of dental plaque and its accessibility for in vivo research makes it one of most studied and bestunderstood biofilm communities. It is now well documented that gram-negative anaerobic bacteria play a significant role in the development of periodontitis, with Porphyromonas gingivalis being implicated as one of the major players in the progression of this chronic disease (10,19,30,61). A number of factors are associated with the virulence of the organism, including a variety of proteases, endotoxins, and collegenases and the production of surface structures, such as fimbriae and capsular polysaccharide (38). This opportunistic pathogen also attaches to and invades human epithelial cells (18,53,56,57), connective tissue, and endothelial cells (15,17,55), and invasion has been shown to be mediated by the expression of fimbriae and a variety of surface adhesins. It is evident that the growth of P. gingivalis within the subgingival plaque is central to the disease process; however, although there have been numerous studies of the pathogenicity of the organism and its interactions with other organisms within the biofilm community, little is known about the molecular-genetic basis of biofilm formation in P. gingivalis.Research on oral biofilms has focused on determining the spatial organization and complex development of plaque by examining the succession of organisms in the growing biofilm. By monitoring the development of the microbial community on the tooth surface after professional cleaning, studies have demonstrated that the early colonizers are primarily grampositive organisms and the late, o...

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Section: Isolation Of the Pg0106 Mutantsupporting

confidence: 67%

Section: Isolation Of the Pg0106 Mutantmentioning

confidence: 74%

Section: Discussionmentioning

confidence: 99%

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Enhanced Biofilm Formation and Loss of Capsule Synthesis: Deletion of a Putative Glycosyltransferase inPorphyromonas gingivalis

Davey¹,

Duncan²

2006

J Bacteriol

112

104

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“…The K-antigen capsule of P. gingivalis is considered a key virulence factor (52). Encapsulated strains disseminate, causing a spreading type of infection in mice, with recovery from blood, spleen, and kidneys after subcutaneous inoculation, while K-antigen null strains typically result in localized abscesses and are significantly less virulent in soft tissue destruction (17,31). Also, it was recently reported that mice immunized with purified K-antigen capsule were protected against oral bone loss when challenged with P. gingivalis (24).…”

mentioning

confidence: 99%

“…Also, it was recently reported that mice immunized with purified K-antigen capsule were protected against oral bone loss when challenged with P. gingivalis (24). With regards to interaction with the human host, the presence and type of capsule has been found to influence the initial adhesion of P. gingivalis to human periodontal pocket epithelial cells (17) and to reduce the immune response of human gingival fibroblasts (7). Furthermore, the majority of clinical P. gingivalis strains isolated from patients with destructive periodontal disease synthesize K-antigen capsule (30), indicating a link between the disease state and the proliferation of an encapsulated phenotype.…”

mentioning

confidence: 99%

HU Protein Affects Transcription of Surface Polysaccharide Synthesis Genes in Porphyromonas gingivalis

Alberti-Segui¹,

Arndt²,

Cugini³

et al. 2010

J Bacteriol

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K-antigen capsule synthesis is an important virulence determinant of the oral anaerobe Porphyromonas gingivalis. We previously reported that the locus required for synthesis of this surface polysaccharide in strain W83 (TIGR identification PG0106 to PG0120) is transcribed as a large (ϳ16.7-kb) polycistronic message. Through sequence analysis, we have now identified a 77-bp inverted repeat located upstream (206 bp) of the start codon of PG0106 that is capable of forming a large hairpin structure. Further sequence analysis just upstream and downstream of the capsule synthesis genes revealed the presence of two genes oriented in the same direction as the operon that are predicted to encode DNA binding proteins: PG0104, which is highly similar (57%) to DNA topoisomerase III, and PG0121, which has high similarity (72%) to DNA binding protein HU (␤-subunit). In this report, we show that these two genes, as well as the 77-bp inverted repeat region, are cotranscribed with the capsule synthesis genes, resulting in a large transcript that is ϳ19.4 kb (based on annotation). We also show that a PG0121 recombinant protein is a nonspecific DNA binding protein with strong affinity to the hairpin structure, in vitro, and that transcript levels of the capsule synthesis genes are downregulated in a PG0121 deletion mutant. Furthermore, we show that this decrease in transcript levels corresponds to a decrease in the amount of polysaccharide produced. Interestingly, expression analysis of another polysaccharide synthesis locus (PG1136 to PG1143) encoding genes involved in synthesis of a surfaceassociated phosphorylated branched mannan (APS) indicated that this locus is also downregulated in the PG0121 mutant. Altogether our data indicate that HU protein modulates expression of surface polysaccharides in P. gingivalis strain W83.

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Capsular‐defective Porphyromonas gingivalis mutant strains induce less alveolar bone resorption than W50 wild‐type strain due to a decreased Th1/Th17 immune response and less osteoclast activity

Monasterio

Fernández

Castillo

et al. 2018

Journal of Periodontology

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Background Encapsulation of Porphyromonas gingivalis has been demonstrated as responsible of several host immunological changes, which have been associated with the pathogenesis of periodontitis. Using a murine model of periodontitis and two isogenic non‐capsulated mutants of P. gingivalis, this study aimed to analyze whether P. gingivalis encapsulation induces more severe alveolar bone resorption, and whether this bone loss is associated with a T‐helper (Th)1 and Th17‐pattern of immune response. Methods Experimental periodontal infections were generated by oral inoculation with the encapsulated W50 wild‐type strain or isogenic non‐encapsulated ΔPG0116‐PG0120 (GPA) and ΔPG0109‐PG0118 (GPC) mutants of P. gingivalis. Periodontal infections induced with the encapsulated HG184 or non‐encapsulated ATCC 33277 strains of P. gingivalis were used as controls. Alveolar bone resorption was analyzed using microcomputed tomography and scanning electron microscopy. The expression levels of Th1, Th2, Th17, or T regulatory‐associated cytokines and RANKL, as well as the periodontal bacterial load, were quantified by quantitative polymerase chain reaction. The detection of Th1 and Th17 lymphocytes was analyzed by flow cytometry. Results In the periodontal lesions, both capsular‐defective knockout mutant strains of P. gingivalis induced less alveolar bone resorption than the encapsulated W50 wild‐type strain. This decreased bone loss was associated with a dismissed RANKL expression, decreased Th1‐ and Th17‐type of cytokine expression, reduced Th1 and Th17 lymphocyte detection, and low osteoclast finding. Conclusion These data demonstrate that encapsulation of P. gingivalis plays a key role in the alveolar bone resorption induced during periodontitis, and this bone loss is associated with a Th1‐ and Th17‐pattern of immune response triggered in the periodontal lesions.

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Adhesion of Porphyromonas gingivalis. Serotypes to Pocket Epithelium

Abstract: This study indicates that the presence and type of capsule have a significant influence on the initial adhesion of P. gingivalis to human periodontal pocket epithelial cells.

Cited by 33 publications

References 24 publications

Enhanced Biofilm Formation and Loss of Capsule Synthesis: Deletion of a Putative Glycosyltransferase inPorphyromonas gingivalis

Enhanced Biofilm Formation and Loss of Capsule Synthesis: Deletion of a Putative Glycosyltransferase inPorphyromonas gingivalis

HU Protein Affects Transcription of Surface Polysaccharide Synthesis Genes in Porphyromonas gingivalis

Capsular‐defective Porphyromonas gingivalis mutant strains induce less alveolar bone resorption than W50 wild‐type strain due to a decreased Th1/Th17 immune response and less osteoclast activity

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