Anti-inflammatory effects of olanexidine gluconate on oral epithelial cells.
Keratinocytes
Olanexidine gluconate
Porphyromonas gingivalis lipopolysaccharide
Journal
BMC oral health
ISSN: 1472-6831
Titre abrégé: BMC Oral Health
Pays: England
ID NLM: 101088684
Informations de publication
Date de publication:
08 11 2019
08 11 2019
Historique:
received:
06
01
2019
accepted:
21
10
2019
entrez:
10
11
2019
pubmed:
11
11
2019
medline:
23
2
2020
Statut:
epublish
Résumé
Periodontitis is a biofilm-induced chronic inflammatory condition of the periodontium. Chemokines produced by the innate and acquired immune responses play a significant role in disease progression. Reducing biofilm formation and inflammatory response caused by chemokines is vital for preventing and treating periodontitis. Previously, we observed that treatment with 0.1% olanexidine gluconate (OLG) inhibited biofilm formation on saliva-coated hydroxyapatite. This study aimed to evaluate the anti-inflammatory effect of OLG on oral epithelial cells. We examined if OLG could inhibit the inflammatory responses caused by Porphyromonas gingivalis (P. gingivalis) lipopolysaccharide (LPS) and heat-killed P. gingivalis in immortalized human oral keratinocytes (RT7). Treatment of RT7 with non-cytotoxic OLG concentrations significantly inhibited the production of inflammatory chemokines such as interleukin 8 (IL-8), C-C motif ligand 20 (CCL20), and growth-related oncogene protein-α (GRO-α), which are stimulated by P. gingivalis LPS in a concentration-dependent manner. Moreover, the inhibitory effects were observed regardless of the treatment time with P. gingivalis LPS (6, 12, or 24 h). OLG also significantly inhibited chemokine production stimulated by heat-killed P. gingivalis. The findings of this study suggest that treatment with OLG inhibits chronic inflammatory reactions in oral mucosal cells, such as periodontitis, caused by oral bacteria.
Sections du résumé
BACKGROUND
Periodontitis is a biofilm-induced chronic inflammatory condition of the periodontium. Chemokines produced by the innate and acquired immune responses play a significant role in disease progression. Reducing biofilm formation and inflammatory response caused by chemokines is vital for preventing and treating periodontitis. Previously, we observed that treatment with 0.1% olanexidine gluconate (OLG) inhibited biofilm formation on saliva-coated hydroxyapatite. This study aimed to evaluate the anti-inflammatory effect of OLG on oral epithelial cells.
METHODS
We examined if OLG could inhibit the inflammatory responses caused by Porphyromonas gingivalis (P. gingivalis) lipopolysaccharide (LPS) and heat-killed P. gingivalis in immortalized human oral keratinocytes (RT7).
RESULTS
Treatment of RT7 with non-cytotoxic OLG concentrations significantly inhibited the production of inflammatory chemokines such as interleukin 8 (IL-8), C-C motif ligand 20 (CCL20), and growth-related oncogene protein-α (GRO-α), which are stimulated by P. gingivalis LPS in a concentration-dependent manner. Moreover, the inhibitory effects were observed regardless of the treatment time with P. gingivalis LPS (6, 12, or 24 h). OLG also significantly inhibited chemokine production stimulated by heat-killed P. gingivalis.
CONCLUSIONS
The findings of this study suggest that treatment with OLG inhibits chronic inflammatory reactions in oral mucosal cells, such as periodontitis, caused by oral bacteria.
Identifiants
pubmed: 31703580
doi: 10.1186/s12903-019-0932-0
pii: 10.1186/s12903-019-0932-0
pmc: PMC6839112
doi:
Substances chimiques
Anti-Inflammatory Agents
0
Biguanides
0
Glucuronates
0
Lipopolysaccharides
0
olanexidine gluconate
I69T4JE922
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
239Références
Antimicrob Agents Chemother. 2015 Aug;59(8):4551-9
pubmed: 25987609
J Exp Med. 1990 May 1;171(5):1797-802
pubmed: 2185333
J Dent Res. 2006 Jun;85(6):524-9
pubmed: 16723649
Clin Exp Immunol. 2002 Jun;128(3):548-54
pubmed: 12067311
Periodontol 2000. 1999 Jun;20:168-238
pubmed: 10522227
J Med Microbiol. 2015 Jan;64(Pt 1):32-6
pubmed: 25351713
Nature. 1998 Apr 9;392(6676):565-8
pubmed: 9560152
Infect Immun. 2003 Apr;71(4):1643-9
pubmed: 12654776
BMC Oral Health. 2014 Jun 28;14:80
pubmed: 24972711
Ann Periodontol. 1996 Nov;1(1):821-78
pubmed: 9118282
J Clin Periodontol. 1988 Aug;15(7):415-24
pubmed: 3183067
Oral Microbiol Immunol. 2009 Feb;24(1):1-6
pubmed: 19121062
Arch Oral Biol. 2015 Jun;60(6):845-53
pubmed: 25791329
J Periodontol. 2005 Nov;76(11):1950-9
pubmed: 16274315
J Med Microbiol. 2002 Jan;51(1):27-33
pubmed: 11800468
J Periodontol. 2004 Mar;75(3):370-9
pubmed: 15088874
J Exp Med. 2007 Nov 26;204(12):2803-12
pubmed: 18025126
J Med Microbiol. 2017 May;66(5):678-685
pubmed: 28516852
Adv Immunol. 1994;55:97-179
pubmed: 8304236
J Dent Res. 2011 Nov;90(11):1286-92
pubmed: 21865591
Infect Immun. 2001 Mar;69(3):1477-82
pubmed: 11179315
J Clin Periodontol. 2010 Jan;37(1):24-9
pubmed: 20096064
Oral Microbiol Immunol. 2008 Oct;23(5):425-31
pubmed: 18793367