Biofilm formation by Porphyromonas gingivalis and Streptococcus gordonii

2010 ◽  
Vol 33 (3) ◽  
pp. 323-327 ◽  
Author(s):  
G. S. Cook ◽  
J. W. Costerton ◽  
R. J. Lamont
PLoS ONE ◽  
2011 ◽  
Vol 6 (11) ◽  
pp. e27386 ◽  
Author(s):  
Juhi Bagaitkar ◽  
Carlo A. Daep ◽  
Carol K. Patel ◽  
Diane E. Renaud ◽  
Donald R. Demuth ◽  
...  

2010 ◽  
Vol 54 (11) ◽  
pp. 4694-4698 ◽  
Author(s):  
Jie Wu ◽  
Hua Xie

ABSTRACT The ability to attach to a variety of oral surfaces is an important characteristic of Porphyromonas gingivalis. Previous studies have demonstrated that expression and production of FimA, a major subunit protein of the long fimbriae, is required for P. gingivalis colonization. Here we report that a surface protein, arginine deiminase (ArcA) of Streptococcus cristatus, represses FimA production and inhibits biofilm formation of P. gingivalis. This inhibitory function of ArcA is also observed in the formation of heterotypic P. gingivalis-Streptococcus gordonii biofilms. P. gingivalis is released from streptococcal substrates in the presence of ArcA, likely due to an inhibition of FimA production. This work suggests that ArcA may have the potential to be a specific antibiofilm agent to fight P. gingivalis infections.


2006 ◽  
Vol 74 (5) ◽  
pp. 3002-3005 ◽  
Author(s):  
Cindy A. Capestany ◽  
Masae Kuboniwa ◽  
Il-Young Jung ◽  
Yoonsuk Park ◽  
Gena D. Tribble ◽  
...  

ABSTRACT The oral pathogen Porphyromonas gingivalis expresses a homolog of the internalin family protein InlJ. Inactivation of inlJ reduced monospecies biofilm formation by P. gingivalis. In contrast, heterotypic P. gingivalis-Streptococcus gordonii biofilm formation was enhanced in the InlJ-deficient mutant. The results indicate a nuanced role for InlJ in regulating biofilm accumulations of P. gingivalis.


2003 ◽  
Vol 185 (1) ◽  
pp. 274-284 ◽  
Author(s):  
Roderick McNab ◽  
Suzannah K. Ford ◽  
Azza El-Sabaeny ◽  
Bruno Barbieri ◽  
Guy S. Cook ◽  
...  

ABSTRACT Communication based on autoinducer 2 (AI-2) is widespread among gram-negative and gram-positive bacteria, and the AI-2 pathway can control the expression of genes involved in a variety of metabolic pathways and pathogenic mechanisms. In the present study, we identified luxS, a gene responsible for the synthesis of AI-2, in Streptococcus gordonii, a major component of the dental plaque biofilm. S. gordonii conditioned medium induced bioluminescence in an AI-2 reporter strain of Vibrio harveyi. An isogenic mutant of S. gordonii, generated by insertional inactivation of the luxS gene, was unaffected in growth and in its ability to form biofilms on polystyrene surfaces. In contrast, the mutant strain failed to induce bioluminescence in V. harveyi and was unable to form a mixed species biofilm with a LuxS-null strain of the periodontal pathogen Porphyromonas gingivalis. Complementation of the luxS mutation in S. gordonii restored normal biofilm formation with the luxS-deficient P. gingivalis. Differential display PCR demonstrated that the inactivation of S. gordonii luxS downregulated the expression of a number of genes, including gtfG, encoding glucosyltransferase; fruA, encoding extracellular exo-β-d-fructosidase; and lacD encoding tagatose 1,6-diphosphate aldolase. However, S. gordonii cell surface expression of SspA and SspB proteins, previously implicated in mediating adhesion between S. gordonii and P. gingivalis, was unaffected by inactivation of luxS. The results suggest that S. gordonii produces an AI-2-like signaling molecule that regulates aspects of carbohydrate metabolism in the organism. Furthermore, LuxS-dependent intercellular communication is essential for biofilm formation between nongrowing cells of P. gingivalis and S. gordonii.


2003 ◽  
Vol 71 (8) ◽  
pp. 4759-4766 ◽  
Author(s):  
Keeta S. Gilmore ◽  
Pravina Srinivas ◽  
Darrin R. Akins ◽  
Kenneth L. Hatter ◽  
Michael S. Gilmore

ABSTRACT A model for the protracted (30-day) colonization of smooth surfaces by Streptococcus gordonii that incorporates the nutrient flux that occurs in the oral cavity was developed. This model was used to characterize the biphasic expansion of the adherent bacterial population, which corresponded with the emergence of higher-order architectures characteristic of biofilms. Biofilm formation by S. gordonii was observed to be influenced by the presence of simple sugars including sucrose, glucose, and fructose. Real-time PCR was used to quantify changes in expression of S. gordonii genes known or thought to be involved in biofilm formation. Morphological changes were accompanied by a significant shift in gene expression patterns. The majority of S. gordonii genes examined were observed to be downregulated in the biofilm phase. Genes found to be upregulated in the biofilm state were observed to encode products related to environmental sensing and signaling.


2011 ◽  
Vol 80 (1) ◽  
pp. 3-13 ◽  
Author(s):  
Chen Li ◽  
Kurniyati ◽  
Bo Hu ◽  
Jiang Bian ◽  
Jianlan Sun ◽  
...  

ABSTRACTThe oral bacteriumPorphyromonas gingivalisis a key etiological agent of human periodontitis, a prevalent chronic disease that affects up to 80% of the adult population worldwide.P. gingivalisexhibits neuraminidase activity. However, the enzyme responsible for this activity, its biochemical features, and its role in the physiology and virulence ofP. gingivalisremain elusive. In this report, we found thatP. gingivalisencodes a neuraminidase, PG0352 (SiaPg). Transcriptional analysis showed thatPG0352is monocistronic and is regulated by a sigma70-like promoter. Biochemical analyses demonstrated that SiaPgis an exo-α-neuraminidase that cleaves glycosidic-linked sialic acids. Cryoelectron microscopy and tomography analyses revealed that thePG0352deletion mutant (ΔPG352) failed to produce an intact capsule layer. Compared to the wild type,in vitrostudies showed that ΔPG352 formed less biofilm and was less resistant to killing by the host complement.In vivostudies showed that while the wild type caused a spreading type of infection that affected multiple organs and all infected mice were killed, ΔPG352 only caused localized infection and all animals survived. Taken together, these results demonstrate that SiaPgis an important virulence factor that contributes to the biofilm formation, capsule biosynthesis, and pathogenicity ofP. gingivalis, and it can potentially serve as a new target for developing therapeutic agents againstP. gingivalisinfection.


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