<i>Porphyromonas gingivalis</i> suppresses invasion of <i>Fusobacterium nucleatum</i> into gingival epithelial cells

Jung, Young‐Jung; Jun, Hye‐Kyoung; Choi, Bong‐Kyu

doi:10.1080/20002297.2017.1320193

Cited by 23 publications

(30 citation statements)

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“…FadA (Fusobacterium adhesin A), is reported to be required for F. nucleatum attachment to epithelial cells and may play an important role in Fusobacterium colonization in the host [33]. Jung et al reported that the invasion of F. nucleatum into gingival epithelial cells was suppressed in the presence of P. gingivalis [35]. Our results revealed that P. gingivalis could downregulate the expression of fadA in F. nucleatum, which may be a possible explanation of their finding.…”

Section: C2 Vs C3supporting

confidence: 65%

Metatranscriptomic analysis of an in vitro biofilm model reveals strain-specific interactions among multiple bacterial species

Zhang

Shi

Song

et al. 2019

Journal of Oral Microbiology

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Interactions among bacteria can affect biofilm properties. Method: Here, we investigated the role of different bacteria in functional dysbiosis of an in vitro polymicrobial subgingival plaque model using both 16S rRNA and metatranscriptomic sequencing. Results: We found that high-virulence Porphyromonas gingivalis W83 had greater effects on the symbiotic species than the low-virulence P. gingivalis ATCC33277, and that Prevotella intermedia exacerbated the effects of W83. P. gingivalis significantly influenced the expression of genes related to metabolic pathways and quorum sensing of commensal oral species in a strain-specific manner. P. intermedia exerted synergistic effects with P. gingivalis W83 but antagonistic effects with strain ATCC33277, which may regulate the expression of virulence factors of P. gingivalis through the clp regulator. Discussion: The interaction networks indicated that the strongest correlation was between Fusobacterium nucleatum and Streptococcus mitis, which demonstrated their bridge and cornerstone roles in biofilm. Changes in the expression of genes relating to outer membrane proteins in F. nucleatum indicated that the addition of different bacteria can interfere with the co-adherence among F. nucleatum and other partners. Conclusion: We report here the existence of strain-specific interactions in subgingival plaque, which may enhance our understanding of periodontal micro-ecology and facilitate the development of improved plaque control strategies.

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Section: C2 Vs C3supporting

confidence: 65%

Metatranscriptomic analysis of an in vitro biofilm model reveals strain-specific interactions among multiple bacterial species

Zhang

Shi

Song

et al. 2019

Journal of Oral Microbiology

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“…nucleatum and P. gingivalis are the major pathogens that cause periodontitis (Hajishengallis et al, 2012;Yang et al, 2014;Han, 2015;How et al, 2016). Furthermore, coinfection of F. nucleatum and P. gingivalis could enhance their adherence and invasive capacity in human gingival epithelial cells and inhibit the host innate immune response (Li et al, 2015;Jung et al, 2017). Therefore, we tested the antibacterial activity against both planktonic cultures and biofilms.…”

Section: Discussionmentioning

confidence: 99%

Mesoporous Hydroxyapatite/Chitosan Loaded With Recombinant-Human Amelogenin Could Enhance Antibacterial Effect and Promote Periodontal Regeneration

Liao

Shu

et al. 2020

Front. Cell. Infect. Microbiol.

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The recovery of impaired periodontium is still a challenge to the treatment of periodontitis. This study was the first to apply the mesoporous hydroxyapatites/chitosan (mHA/CS) composite scaffold to periodontal regeneration. The aim of our study is to evaluate the biological effects of mesoporous hydroxyapatite/chitosan (mHA/CS) loaded with recombinant human amelogenin (rhAm) on periodontal regeneration. The physicochemical properties of mHA/CS scaffolds were examined by Fourier transform infrared spectroscopy (FTIR), transmission electron microscopy (TEM), and Brunauer-Emmett-Teller (BET) analysis. Then, the biological effects of the mHA/CS loaded with rhAm were evaluated, including antibacterial effect, controlled-release capacity, osteogenic and cementogenic effects in vitro and in vivo. The antibacterial effect was tested on 1.5 mg/mL CS; 3 mg/mL mHA; 2.25 mg/mL mHA/CS; 4.5 mg/mL mHA/CS and 20 µg/mL rhAm. Tryptic Soy Broth culture medium was used as a baseline control. Osteogenic effect of rhAm (20 µg/mL rhAm), mHA/CS (4.5 mg/mL mHA/CS), and mHA/CS-rhAm (4.5 mg/mL mHA/CS and 20 µg/mL rhAm) on human periodontal ligament cells (hPDLCs) was evaluated in osteogenic media. The hPDLCs treated either with osteogenic media or Dulbecco's modified Eagle's medium (DMEM) alone were used as the baseline control. In the animal model, 4week-old nude mice (BALB/c) (n = 6) implanted with root slices subcutaneously were used to observe the cementogenic effect in vivo. The root slices were treated with rhAm (20 µg/mL rhAm), mHA/CS (4.5 mg/mL mHA/CS), and mHA/CS-rhAm (4.5 mg/mL mHA/CS and 20 µg/mL rhAm). The root slices treated with osteogenic medium alone were used as the baseline control. The analyses showed that the mHA/CS particles were 2 µm in diameter and had a uniform pore size. Liao et al. A Research on Periodontal Regeneration The mesoporous structure was 7 nm in diameter and its surface area was 33.95 m 2 /g. The scaffold exhibited antibacterial effects against Fusobacterium nucleatum and Porphyromonas gingivalis. The mHA/CS scaffold sustainably released rhAm. The mHA/CS loaded with 20 µg/mL rhAm upregulated ALP activity, the expression levels of osteogenesis-related genes and proteins in vitro. Additionally, it promoted the formation of cementum-like tissue in vivo. Our findings suggest that mHA/CS loaded with 20 µg/mL rhAm could inhibit the growth of periodontal pathogens and promote the formation of bone and cementum-like tissue.

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“…The addition of F nucleatum did not significantly affect the amount of invading P gingivalis . Jung et al recently demonstrated that P gingivalis differentially suppresses F nucleatum invasion to immortalized gingival epithelial cells in a gingipain‐dependent manner, and that the effect resulted from specific interactions among P gingivalis, F nucleatum, and the cell type. The different results obtained by Jung et al may derive from the difference in MOI in the different studies, and Jung et al used an MOI of 500 for both bacteria, in contrast to our study that used MOI 100 for P gingivalis and MOI 10 for F nucleatum .…”

Section: Discussionmentioning

confidence: 99%

Myd88 plays a major role in the keratinocyte response to infection with Porphyromonas gingivalis

Polak

Zigron

Eli-Berchoer

et al. 2019

J of Periodontal Research

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Aim To explore the role of keratinocyte myeloid differentiation primary response 88 (MyD88) expression in the adhesion of Porphyromonas gingivalis to the cells and its subsequent invasion and intracellular survival. Materials and Methods Primary mouse keratinocytes from wild‐type (WT) or Myd88−/− mice were infected with P gingivalis alone or co‐infected with Fusobacterium nucleatum. Bacterial adhesion and invasion were measured using fluorescent microscopy and flow cytometry, and intracellular survival in keratinocytes was quantified by an antibiotic protection assay. Keratinocyte expression of antimicrobial peptides was measured by real‐time PCR. Results In the absence of MyD88, P gingivalis adherence, invasion, and intracellular survival were enhanced compared with WT keratinocytes. The presence of F nucleatum during infection increased the adhesion of P gingivalis to WT keratinocytes but reduced the adhesion to Myd88−/− keratinocytes. Fusobacterium nucleatum improved mildly the invasion and survival of P gingivalis in both cell types. Baseline expression of beta‐defensin 2, 3, 4 and RegIII‐γ was elevated in Myd88−/− keratinocytes compared to WT cells; however, following infection beta‐defensin expression was strongly induced in WT cells but decreased dramatically in the MyD88 deficient cells. Conclusion In the absence of MyD88 expression, P gingivalis adhesion to keratinocytes is improved, and invasion and intracellular survival are increased. Furthermore, keratinocyte infection by P gingivalis induces antimicrobial peptide expression in a MyD88‐dependent manner. Thus, MyD88 plays a key role in the interaction between P gingivalis and keratinocytes.

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Porphyromonas gingivalis suppresses invasion of Fusobacterium nucleatum into gingival epithelial cells

Cited by 23 publications

References 50 publications

Metatranscriptomic analysis of an in vitro biofilm model reveals strain-specific interactions among multiple bacterial species

Metatranscriptomic analysis of an in vitro biofilm model reveals strain-specific interactions among multiple bacterial species

Mesoporous Hydroxyapatite/Chitosan Loaded With Recombinant-Human Amelogenin Could Enhance Antibacterial Effect and Promote Periodontal Regeneration

Myd88 plays a major role in the keratinocyte response to infection with Porphyromonas gingivalis

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