<i>Porphyromonas gingivalis</i>
            Minor Fimbriae Are Required for Cell-Cell Interactions

Lin, Xinghua; Wu, Jie; Xie, Hua

doi:10.1128/iai.00797-06

Cited by 69 publications

(77 citation statements)

References 19 publications

(12 reference statements)

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“…Studies have demonstrated a role for long fimbriae in adherence to and invasion of gingival epithelial cells, bone resorption, co-aggregation with other oral isolates, and biofilm formation (Amano et al, 2004;Hamada et al, 1998;Lamont & Jenkinson, 1998). Interestingly, it was recently shown that the short fimbriae, unlike the long fimbriae, are required for autoaggregation (Lin et al, 2006), indicating that these two surface structures have distinctive functions. The in vivo signals that trigger the expression of genes involved in the biogenesis of fimbriae are not known; however, it has been shown that expression is affected by environmental and nutritional parameters.…”

Section: Discussionmentioning

confidence: 99%

A streptococcal effector protein that inhibits Porphyromonas gingivalis biofilm development

Christopher¹,

Arndt

Cugini³

et al. 2010

Microbiology

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Dental plaque formation is a developmental process involving cooperation and competition within a diverse microbial community, approximately 70 % of which is composed of an array of streptococci during the early stages of supragingival plaque formation. In this study, 79 cell-free culture supernatants from a variety of oral streptococci were screened to identify extracellular compounds that inhibit biofilm formation by the oral anaerobe Porphyromonas gingivalis strain 381. The majority of the streptococcal supernatants (61 isolates) resulted in lysis of P. gingivalis cells, and some (17 isolates) had no effect on cell viability, growth or biofilm formation. One strain, however, produced a supernatant that abolished biofilm formation without affecting growth rate. Analysis of this activity led to the discovery that a 48 kDa protein was responsible for the inhibition. Protein sequence identification and enzyme activity assays identified the effector protein as an arginine deiminase. To identify the mechanism(s) by which this protein inhibits biofilm formation, we began by examining the expression levels of genes encoding fimbrial subunits; surface structures known to be involved in biofilm development. Quantitative RT-PCR analysis revealed that exposure of P. gingivalis cells to this protein for 1 h resulted in the downregulation of genes encoding proteins that are the major subunits of two distinct types of thin, single-stranded fimbriae (fimA and mfa1). Furthermore, this downregulation occurred in the absence of arginine deiminase enzymic activity. Hence, our data indicate that P. gingivalis can sense this extracellular protein, produced by an oral streptococcus (Streptococcus intermedius), and respond by downregulating expression of cell-surface appendages required for attachment and biofilm development. INTRODUCTIONHigh cell density and microbial diversity are fundamental to the development and function of the oral biofilm (Kolenbrander et al., 2002). The close proximity of cells within the biofilm facilitates cell-cell interactions, while the diversity offers a wide variety of metabolic functions, allowing the community to acquire nutrients and persist. During plaque formation, organisms affect the activities of one another via physical associations and through the release of extracellular molecules; the effects of these interactions range from mutualistic to antagonistic (Davey & Costerton, 2006;Socransky & Haffajee, 2000). Molecules that are excreted by bacteria into the environment or directly into host cells (through either non-classical or conventional secretion pathways), affecting gene expression of another organism, are often referred to as effectors. The primary objective of this study was to identify effectors produced by oral streptococci that modulate biofilm formation by the oral anaerobe Porphyromonas gingivalis. P. gingivalis is a Gram-negative anaerobe that persists within the oral biofilm community. Outgrowth of this normally commensal organism is associated with severe periodontal disease, r...

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Section: Discussionmentioning

confidence: 99%

A streptococcal effector protein that inhibits Porphyromonas gingivalis biofilm development

Christopher¹,

Arndt

Cugini³

et al. 2010

Microbiology

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“…CLSM analysis of the biofilms formed by the ATCC 33277 fimR and fimS mutants showed that they produced biofilms that were distinct from the wild-type strain and also from each other, with rough and heterogeneous biofilms suggesting an apparent reduction of microcolony contacts. In vitro analysis of ATCC 33277 fimA and mfa1 mutants has shown FimA to be involved in adhesion of P. gingivalis to saliva-coated glass surfaces (26) and cultured KB epithelial cells (51), while mfa1 expression mediates cell aggregation (26). Neither the fimA nor mfa1 mutants formed a confluent biofilm (26).…”

Section: Discussionmentioning

confidence: 99%

“…The expression of genes important for P. gingivalis fimbriation in the fimS and fimR mutants. It has been shown that production of the fimbrillins Mfa1 and FimA is essential for biofilm formation by P. gingivalis ATCC 33277 (26). Furthermore, it has been shown that FimR binds directly to the mfa1 promoter region (54) and to the promoter of the fimbriationassociated gene fimX that is upstream of fimA (37) (annotated as pg2130 in the W83 genome [36] and pgn_0178 in the recently released ATCC 33277 genome sequence [34]).…”

Section: Vol 192 2010 Fimr and Fims In P Gingivalis Biofilm 1337mentioning

confidence: 99%

“…Given the variation in surfaces to which P. gingivalis may attach, it is likely that numerous cell structures are required to mediate the interactions necessary for specific and stable adherence. Indeed, recent studies have shown that both the major fimbrillin FimA and the minor fimbrillin Mfa1 are required for full P. gingivalis biofilm development by strain ATCC 33277 (26). In addition, the involvement of capsular polysaccharide and lipopolysaccharide O antigen has been implicated in P. gingivalis biofilm formation (10,35).…”

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confidence: 99%

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FimR and FimS: Biofilm Formation and Gene Expression inPorphyromonas gingivalis

Seers

Dashper

et al. 2010

J Bacteriol

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Porphyromonas gingivalis is a late-colonizing bacterium of the subgingival dental plaque biofilm associated with periodontitis. Two P. gingivalis genes, fimR and fimS, are predicted to encode a two-component signal transduction system comprising a response regulator (FimR) and a sensor histidine kinase (FimS). In this study, we show that fimS and fimR, although contiguous on the genome, are not part of an operon. We inactivated fimR and fimS in both the afimbriated strain W50 and the fimbriated strain ATCC 33277 and demonstrated that both mutants formed significantly less biofilm than their respective wild-type strains. Quantitative reverse transcription-real-time PCR showed that expression of fimbriation genes was reduced in both the fimS and fimR mutants of strain ATCC 33277. The mutations had no effect, in either strain, on the P. gingivalis growth rate or on the response to hydrogen peroxide or growth at pH 9, at 41°C, or at low hemin availability. Transcriptome analysis using DNA microarrays revealed that inactivation of fimS resulted in the differential expression of 10% of the P. gingivalis genome (>1.5-fold; P < 0.05). Notably genes encoding seven different transcriptional regulators, including the fimR gene and three extracytoplasmic sigma factor genes, were differentially expressed in the fimS mutant.Two-component signal transduction systems (TCSTS) are used by bacteria to control the expression of a range of genes in response to a variety of environmental and intracellular stimuli. These systems are found in almost all bacteria and are known to regulate an array of physiological traits, including osmoregulation (4), virulence (8), and quorum sensing (21). The crucial role of TCSTS in governing the signaling and regulatory pathways associated with biofilm development has been well documented in many bacteria, including Escherichia coli, Pseudomonas aeruginosa, and Streptococcus mutans (11,25,39). Typically, each TCSTS functions via a phosphorylation cascade and consists of a membrane-bound or cytoplasmic sensor histidine kinase (SHK), which perceives a particular stimulus, and a cytoplasmic response regulator (RR), which allows the cell to respond to the stimulus accordingly via regulation of gene expression (49).Porphyromonas gingivalis is a Gram-negative anaerobe that has been strongly implicated as a major etiologic agent in the onset and progression of chronic periodontitis (47, 55), a disease of the supporting tissues of the teeth. P. gingivalis is a late colonizer of subgingival dental plaque, a complex and dynamic polymicrobial biofilm (22, 31), and its ability to persist as part of a subgingival plaque biofilm is dependent on its adherence to and colonization of the subgingival niche. P. gingivalis has been shown to adhere to primary plaque-colonizing species, particularly Streptococcus spp. such as Streptococcus gordonii (24,29,33,48). Binding of P. gingivalis to S. gordonii has been shown to result in the formation of a bispecies biofilm with P. gingivalis attached to S. gordonii bound to a s...

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“…Two distinctly different fimbriae are present on the P. ginigvalis cells; major or long, a 49 kDa protein, encoded by fimA gene and minor or short fimbriae composed of 67 kDa protein, encoded by mfa1 gene. [29]. It has been shown that fimbriae activate both humoral and cellular responses and inactivation of fimA gene reduces periodontal bone loss in gnotobiotic rats.…”

Section: Virulence Factors Of P Gingivalismentioning

confidence: 99%

Periodontitis- A Review

Shah¹

2017

Med Clin Rev

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The early form of periodontitis is gingivitis where inflammatory changes including bleeding and swelling are restricted to marginal gingiva and surrounding connective tissue, without the involvement of periodontal ligament. Periodontitis occurs when inflammatory changes reach the periodontal ligament and alveolar bone ultimately leading to tooth loss. The underlying cause of the disease is the presence of a polymicrobial biofilm that forms as plaque on the tooth surface and the resulting host response that this plaque induces. Inflammatory responses are initiated by a number of late stage colonizers and the virulence factors they produce. Among these late stage pathogens is P. gingivalis, a Gram negative, asacchrolytic bacterium with a large arsenal of virulence factors. P. gingivalis produces up to 13 virulence factors involved in host evasion and 21 virulence factors involved in tissue destruction. The presence of these virulence factors induces the production of proinflammatory chemokine and cytokine responses often seen in the saliva and gingival crevicular fluid of individuals with periodontitis.

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Porphyromonas gingivalis Minor Fimbriae Are Required for Cell-Cell Interactions

Cited by 69 publications

References 19 publications

A streptococcal effector protein that inhibits Porphyromonas gingivalis biofilm development

A streptococcal effector protein that inhibits Porphyromonas gingivalis biofilm development

FimR and FimS: Biofilm Formation and Gene Expression inPorphyromonas gingivalis

Periodontitis- A Review

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