Smokeless Tobacco Effects on Monocyte Secretion of PGE2 and IL‐1β

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Abstract
The use of smokeless tobacco (st) products is associated with mucosal lesions, gingival recession, and attachment loss at the site of tobacco placement. Monocytes/macrophages are primary producers of PGE2 and IL‐1β, inflammatory mediators which are thought to play a role in the destruction of the periodontium. The purpose of this study was to determine the effect of ST alone and in combination with a major stimulator of inflammation, bacterial lipopolysaccharide (LPS), on monocyte secretion of these mediators. Peripheral blood monocytes (PBM) were isolated by counterflow centrifugal elutriation from 15 healthy donors who were non‐ST users. PBM were incubated for 24 hours in RPMI 1640 containing various concentrations of ST (0%, 0.005%, 0.01%, 1%) with or without 10 μg/ml LPS (Porphyromonas gingivalis LPS or Escherichia coli LPS). Of the ST preparations, only 1% ST resulted in PBM mediator secretion (7.7 ± 2.0 ng/ml for PGE2 and 1.3 ± 0.2 ng/ml for IL‐1β) above that of control (unstimulated) cultures. Furthermore, the combination of 1% ST and LPS resulted in a potentiation of PGE2 release (5‐fold for E. coli LPS + 1% ST and 10‐fold for P. gingivalis LPS + 1% ST; P < 0.0001, one‐way ANOVA) relative to the LPS preparations alone. In contrast, PBM IL‐1β release decreased more than 2‐fold upon E. coli LPS and 1% ST exposure, relative to treatment with E. coli LPS alone (P < 0.0001, one‐way ANOVA). PBM IL‐1β release either increased or decreased following treatment with P. gingivalis LPS + 1% ST, depending on the magnitude of the P. gingivalis LPS response alone. These data indicate that ST has profound effects on monocyte secretion of PGE2 and IL‐1β, and modulates the LPS‐mediated monocyte response. J Periodontol 1994;65:937–941.