Porphyromonas gingivalis and Escherichia coli lipopolysaccharide causes resistin release from neutrophils
Version of Record online: 22 OCT 2012
© 2012 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd
Volume 19, Issue 5, pages 479–483, July 2013
How to Cite
Oral Diseases (2013) 19, 479–483
- Issue online: 28 MAY 2013
- Version of Record online: 22 OCT 2012
- Accepted manuscript online: 26 SEP 2012 07:35AM EST
- Manuscript Accepted: 17 SEP 2012
- Manuscript Revised: 11 SEP 2012
- Manuscript Received: 30 JAN 2012
- Nagasaki University
- Grant-in-Aid. Grant Numbers: 21592655, 22592338
It was reported that periodontitis is associated with increased serum resistin levels. We examined whether there was a difference between the release of resistin from neutrophils incubated lipopolysaccharide (LPS) from Porphyromonas gingivalis and with LPS from Escherichia coli, and which cell-surface receptors and intracellular kinases were involved in this process.
Several concentrations of P. gingivalis-LPS and E. coli-LPS were added to neutrophils, supernatant from cultured neutrophils was collected, and resistin levels were measured by ELISA. To examine signaling pathways, neutrophils were pretreated with monoclonal antibodies against CD14, CD18, TLR2, and TLR4, and specific inhibitors of PI3K and MAPKs.
Resistin release from neutrophils was induced both by P. gingivalis-LPS and E. coli-LPS, but resistin release by P. gingivalis-LPS was weaker than E. coli-LPS in low concentrations. Resistin release was decreased by pretreatment with monoclonal antibodies against CD14, CD18, and TLR4, but not by TLR2. Moreover, it was decreased by inhibitors of PI3K, JNK, and p38 MAPK, but not by ERK1/2.
Resistin release from neutrophils was induced by both P. gingivalis-LPS and E. coli-LPS. This was decreased by CD14, CD18, and TLR4 and was dependent on PI3K, JNK, and p38 MAPK, but not on ERK1/2 in intracellular pathways of neutrophils.