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The impact of virulence factors of Porphyromonas gingivalis on wound healing in vitro.

Laheij AM, van Loveren C, Deng D, de Soet JJ - J Oral Microbiol (2015)

Bottom Line: The presence of a capsular polysaccharide lowered significantly the inhibition of epithelial cell migration, while gingipain activity significantly increased the inhibition of cell migration.LPS and the major fimbriae did not influence epithelial cell migration.The capsular polysaccharide and the Arg- and Lys- gingipains of P. gingivalis influenced the capacity of P. gingivalis to hinder wound healing, while LPS and the major fimbriae had no effect.

View Article: PubMed Central - PubMed

Affiliation: Department of Preventive Dentistry, Academic Centre for Dentistry Amsterdam (ACTA), University of Amsterdam and VU University Amsterdam, Amsterdam, The Netherlands; a.laheij@acta.nl.

ABSTRACT

Background: Porphyromonas gingivalis inhibits oral epithelial wound healing in vitro more strongly than other oral bacteria, but it is unknown why P. gingivalis is such a potent inhibitor of wound healing.

Objective: Therefore, the aim of this study was to investigate the influence of major virulence factors of P. gingivalis on wound healing in an in vitro wound-healing model. The influence of the capsular polysaccharide, the Arg- and Lys- gingipains, the major fimbriae and lipopolysaccharide (LPS) was investigated.

Design: A standardized scratch was made in a confluent layer of human oral epithelial cells HO-1-N-1. The epithelial cells were then challenged with different concentrations of several P. gingivalis wild-type strains and knockout mutants. Closure of the scratch was determined after 17 h and compared to control conditions without bacteria.

Results: The P. gingivalis strains ATCC 33277, W83, and W50 significantly inhibited wound healing. The presence of a capsular polysaccharide lowered significantly the inhibition of epithelial cell migration, while gingipain activity significantly increased the inhibition of cell migration. LPS and the major fimbriae did not influence epithelial cell migration. None of the tested P. gingivalis strains completely prevented the inhibition of cell migration, suggesting that other characteristics of P. gingivalis also play a role in the inhibition of wound healing, and that further research is needed.

Conclusions: The capsular polysaccharide and the Arg- and Lys- gingipains of P. gingivalis influenced the capacity of P. gingivalis to hinder wound healing, while LPS and the major fimbriae had no effect.

No MeSH data available.


Related in: MedlinePlus

Mean relative closure (±SEM) from all biological replicates of scratches in oral epithelial cells challenged with heat-inactivated and viable P. gingivalis strains ATCC 33277, W83, and W50. a=significantly different from control (p<0.0083). b=significantly different from MOI 100 of the same strain (p<0.0083). c=significantly different from MOI 1,000 of the same strain (p<0.0083). *=significantly different from ATCC 33277 of the same MOI (p<0.05). #=significantly different from heat-inactivated P. gingivalis of the same MOI and strain (p<0.05).
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Figure 0002: Mean relative closure (±SEM) from all biological replicates of scratches in oral epithelial cells challenged with heat-inactivated and viable P. gingivalis strains ATCC 33277, W83, and W50. a=significantly different from control (p<0.0083). b=significantly different from MOI 100 of the same strain (p<0.0083). c=significantly different from MOI 1,000 of the same strain (p<0.0083). *=significantly different from ATCC 33277 of the same MOI (p<0.05). #=significantly different from heat-inactivated P. gingivalis of the same MOI and strain (p<0.05).

Mentions: The heat-inactivated P. gingivalis strains ATCC 33277, W83, and W50 significantly inhibited the migration of oral epithelial cells at all tested MOIs compared to control in a dose-responsive manner, although the inhibition by the heat-inactivated W83 at MOI 10 did not reach statistical significance (Fig. 2). Viable P. gingivalis ATCC 33277, W83, and W50 significantly inhibited the migration of oral epithelial cells at all tested MOIs compared to control in a dose-responsive manner as well (Fig. 2). Viable W83 and W50 inhibited cell migration more than their heat-inactivated variants (not statistically significant for W50 at MOI 10); however, no differences were found between heat-inactivated and viable P. gingivalis ATCC 33277 (p>0.05).


The impact of virulence factors of Porphyromonas gingivalis on wound healing in vitro.

Laheij AM, van Loveren C, Deng D, de Soet JJ - J Oral Microbiol (2015)

Mean relative closure (±SEM) from all biological replicates of scratches in oral epithelial cells challenged with heat-inactivated and viable P. gingivalis strains ATCC 33277, W83, and W50. a=significantly different from control (p<0.0083). b=significantly different from MOI 100 of the same strain (p<0.0083). c=significantly different from MOI 1,000 of the same strain (p<0.0083). *=significantly different from ATCC 33277 of the same MOI (p<0.05). #=significantly different from heat-inactivated P. gingivalis of the same MOI and strain (p<0.05).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4491305&req=5

Figure 0002: Mean relative closure (±SEM) from all biological replicates of scratches in oral epithelial cells challenged with heat-inactivated and viable P. gingivalis strains ATCC 33277, W83, and W50. a=significantly different from control (p<0.0083). b=significantly different from MOI 100 of the same strain (p<0.0083). c=significantly different from MOI 1,000 of the same strain (p<0.0083). *=significantly different from ATCC 33277 of the same MOI (p<0.05). #=significantly different from heat-inactivated P. gingivalis of the same MOI and strain (p<0.05).
Mentions: The heat-inactivated P. gingivalis strains ATCC 33277, W83, and W50 significantly inhibited the migration of oral epithelial cells at all tested MOIs compared to control in a dose-responsive manner, although the inhibition by the heat-inactivated W83 at MOI 10 did not reach statistical significance (Fig. 2). Viable P. gingivalis ATCC 33277, W83, and W50 significantly inhibited the migration of oral epithelial cells at all tested MOIs compared to control in a dose-responsive manner as well (Fig. 2). Viable W83 and W50 inhibited cell migration more than their heat-inactivated variants (not statistically significant for W50 at MOI 10); however, no differences were found between heat-inactivated and viable P. gingivalis ATCC 33277 (p>0.05).

Bottom Line: The presence of a capsular polysaccharide lowered significantly the inhibition of epithelial cell migration, while gingipain activity significantly increased the inhibition of cell migration.LPS and the major fimbriae did not influence epithelial cell migration.The capsular polysaccharide and the Arg- and Lys- gingipains of P. gingivalis influenced the capacity of P. gingivalis to hinder wound healing, while LPS and the major fimbriae had no effect.

View Article: PubMed Central - PubMed

Affiliation: Department of Preventive Dentistry, Academic Centre for Dentistry Amsterdam (ACTA), University of Amsterdam and VU University Amsterdam, Amsterdam, The Netherlands; a.laheij@acta.nl.

ABSTRACT

Background: Porphyromonas gingivalis inhibits oral epithelial wound healing in vitro more strongly than other oral bacteria, but it is unknown why P. gingivalis is such a potent inhibitor of wound healing.

Objective: Therefore, the aim of this study was to investigate the influence of major virulence factors of P. gingivalis on wound healing in an in vitro wound-healing model. The influence of the capsular polysaccharide, the Arg- and Lys- gingipains, the major fimbriae and lipopolysaccharide (LPS) was investigated.

Design: A standardized scratch was made in a confluent layer of human oral epithelial cells HO-1-N-1. The epithelial cells were then challenged with different concentrations of several P. gingivalis wild-type strains and knockout mutants. Closure of the scratch was determined after 17 h and compared to control conditions without bacteria.

Results: The P. gingivalis strains ATCC 33277, W83, and W50 significantly inhibited wound healing. The presence of a capsular polysaccharide lowered significantly the inhibition of epithelial cell migration, while gingipain activity significantly increased the inhibition of cell migration. LPS and the major fimbriae did not influence epithelial cell migration. None of the tested P. gingivalis strains completely prevented the inhibition of cell migration, suggesting that other characteristics of P. gingivalis also play a role in the inhibition of wound healing, and that further research is needed.

Conclusions: The capsular polysaccharide and the Arg- and Lys- gingipains of P. gingivalis influenced the capacity of P. gingivalis to hinder wound healing, while LPS and the major fimbriae had no effect.

No MeSH data available.


Related in: MedlinePlus