Nicotine effects on PGE 2 and IL‐1β release by LPS‐treated human monocytes

Cigarette smoking is a major risk factor in the development and further progression of periodontitis. However, little is known regarding the pathogenesis of smoking‐related periodontal diseases. The purpose of this study was to examine the effects of nicotine, alone and in combination with lipopolysaccharide (LPS), on monocyte secretion of bone‐resorbing factors, PGE 2 and IL‐1β. Peripheral blood monocytes (PBM) were isolated by counterflow centrifugal elutriation from 15 healthy, non‐smoking donors. PBM were incubated for 24 h in RPMI 1640 containing nicotine (0, 50 μg/ml, I μg/ml, 10 μg/ml and 100 μg/ml) with or without 10 μg/ml Porphyromonas gingivalis LPS or Escherichia coli LPS. Culture supernatants were assayed for PGE 2 and IL‐1β by ELISA. None of the nicotine preparations resulted in significant PBM secretion of PGE 2 and IL‐1β above that of unstimulated cultures. However, PGE 2 release was potentiated 1.7‐fold by the combination of P. gingivalis LPS and 10 μg/ml nicotine relative to P. gingivalis LPS alone (p<0.05, one‐way ANOVA). Prostaglandin E 3 release also was potentiated 3.5‐fold by P. gingivalis LPS and 100 μg/ml nicotine relative to P. gingivalis LPS alone (p<0.00001, one‐way ANOVA) and 3.1‐fold by E. coli LPS and 100 μg/ml nicotine relative to E. coli LPS alone (p<0.00001, I. one‐way ANOVA). IL‐1β secretion was lower for either LPS plus 100 μg/ml nicotine relative to LPS alone, although not significantly. These data demonstrate upregulation of LPS‐mediated monocyte secretion of PGE 2 by nicotine and suggest a potential role for nicotine in periodontal disease pathogenesis.