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Keywords:

  • neutrophil;
  • resistin;
  • lipopolysaccharide

Objectives

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.

Methods

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.

Results

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.

Conclusions

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.