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Differential effects of LPS from Escherichia coli and Porphyromonas gingivalis on IL-6 production in human periodontal ligament cells.

Nebel, Daniel LU ; Arvidsson, Joel LU ; Lillqvist, Johan; Holm, Anders LU and Nilsson, Bengt-Olof LU (2013) In Acta Odontologica Scandinavica 71(3-4). p.892-898
Abstract
Abstract Objective. Periodontal ligament (PDL) cells produce IL-6 upon stimulation with inflammation promoters, but the signaling pathways involved have not been characterized. This study investigates underlying mechanisms behind regulation of PDL cell IL-6 production by E. coli and P. gingivalis LPS. Materials and methods: Human PDL cells, endothelial cells and monocytes were stimulated with E. coli or P. gingivalis LPS in the presence or absence of pharmacological agents in order to disclose pathways involved in LPS signaling. Gene expression and cellular protein levels were assessed by quantitative real-time PCR and ELISA, respectively. Results. Stimulation with LPS from E. coli (1 µg/ml) for 24 h enhanced PDL cell IL-6 expression... (More)
Abstract Objective. Periodontal ligament (PDL) cells produce IL-6 upon stimulation with inflammation promoters, but the signaling pathways involved have not been characterized. This study investigates underlying mechanisms behind regulation of PDL cell IL-6 production by E. coli and P. gingivalis LPS. Materials and methods: Human PDL cells, endothelial cells and monocytes were stimulated with E. coli or P. gingivalis LPS in the presence or absence of pharmacological agents in order to disclose pathways involved in LPS signaling. Gene expression and cellular protein levels were assessed by quantitative real-time PCR and ELISA, respectively. Results. Stimulation with LPS from E. coli (1 µg/ml) for 24 h enhanced PDL cell IL-6 expression several fold, demonstrated both on transcript and protein levels, but P. gingivalis LPS (1-5 µg/ml) had no effect. TLR2 mRNA was more highly expressed than TLR4 transcript in PDL cells. Treatment with the non-selective nitric oxide synthase inhibitor L-NAME (100 µM) reduced E. coli LPS-induced PDL cell IL-6 by 30%, while neither aminoguanidine (10 µM), an inhibitor of inducible nitric oxide synthase, nor estrogen (17β-estradiol, 100 nM) influenced IL-6. Treatment with the glucocorticoid dexamethasone (1 µM) totally prevented the E. coli LPS-induced PDL cell IL-6. In endothelial cells, neither E. coli LPS nor P. gingivalis LPS promoted IL-6 production. In monocytes, serving as positive control, both E. coli and P. gingivalis LPS stimulated IL-6. Conclusions. E. coli LPS but not P. gingivalis LPS stimulates PDL cell IL-6 production through a glucocorticoid-sensitive mechanism involving nitric oxide formation, probably via endothelial nitric oxide synthase. (Less)
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type
Contribution to journal
publication status
published
subject
in
Acta Odontologica Scandinavica
volume
71
issue
3-4
pages
892 - 898
publisher
Taylor & Francis
external identifiers
  • wos:000322832200076
  • pmid:23116357
  • scopus:84877303476
ISSN
1502-3850
DOI
10.3109/00016357.2012.734415
language
English
LU publication?
yes
id
686dfd41-3e29-4851-aa53-2c2485d78ecf (old id 3219330)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/23116357?dopt=Abstract
date added to LUP
2012-12-03 11:54:01
date last changed
2019-04-10 01:23:06
@article{686dfd41-3e29-4851-aa53-2c2485d78ecf,
  abstract     = {Abstract Objective. Periodontal ligament (PDL) cells produce IL-6 upon stimulation with inflammation promoters, but the signaling pathways involved have not been characterized. This study investigates underlying mechanisms behind regulation of PDL cell IL-6 production by E. coli and P. gingivalis LPS. Materials and methods: Human PDL cells, endothelial cells and monocytes were stimulated with E. coli or P. gingivalis LPS in the presence or absence of pharmacological agents in order to disclose pathways involved in LPS signaling. Gene expression and cellular protein levels were assessed by quantitative real-time PCR and ELISA, respectively. Results. Stimulation with LPS from E. coli (1 µg/ml) for 24 h enhanced PDL cell IL-6 expression several fold, demonstrated both on transcript and protein levels, but P. gingivalis LPS (1-5 µg/ml) had no effect. TLR2 mRNA was more highly expressed than TLR4 transcript in PDL cells. Treatment with the non-selective nitric oxide synthase inhibitor L-NAME (100 µM) reduced E. coli LPS-induced PDL cell IL-6 by 30%, while neither aminoguanidine (10 µM), an inhibitor of inducible nitric oxide synthase, nor estrogen (17β-estradiol, 100 nM) influenced IL-6. Treatment with the glucocorticoid dexamethasone (1 µM) totally prevented the E. coli LPS-induced PDL cell IL-6. In endothelial cells, neither E. coli LPS nor P. gingivalis LPS promoted IL-6 production. In monocytes, serving as positive control, both E. coli and P. gingivalis LPS stimulated IL-6. Conclusions. E. coli LPS but not P. gingivalis LPS stimulates PDL cell IL-6 production through a glucocorticoid-sensitive mechanism involving nitric oxide formation, probably via endothelial nitric oxide synthase.},
  author       = {Nebel, Daniel and Arvidsson, Joel and Lillqvist, Johan and Holm, Anders and Nilsson, Bengt-Olof},
  issn         = {1502-3850},
  language     = {eng},
  number       = {3-4},
  pages        = {892--898},
  publisher    = {Taylor & Francis},
  series       = {Acta Odontologica Scandinavica},
  title        = {Differential effects of LPS from Escherichia coli and Porphyromonas gingivalis on IL-6 production in human periodontal ligament cells.},
  url          = {http://dx.doi.org/10.3109/00016357.2012.734415},
  volume       = {71},
  year         = {2013},
}