The release of interleukin-1 beta, tumor necrosis factor-alpha and interferon-gamma by cultured peripheral blood mononuclear cells from patients with periodontitis.

The extracellular release of IL-1 beta by cultured peripheral blood monocytes from 26 periodontitis patients and 26 control subjects was measured by radioimmunoassay. Unstimulated monocytes from periodontitis patients released significantly more IL-1 beta than controls during 24 h of culture; there was a wide variation in the amount of IL-1 beta released (0.45-13.00 ng/ml per 10(6) cells) which did not correlate with either the degree of bone loss or pocket formation observed clinically. When stimulated with lipopolysaccharide (LPS; Actinobacillus actinomycetemcomitans; 5 micrograms/ml) monocytes from periodontitis patients produced significantly more IL-1 beta than those from control subjects. Monocyte culture supernatants from another 10 periodontitis patients and 10 control subjects were also assayed for both IL-1 beta and TNF-alpha by enzyme-linked immunosorbent assays. Spontaneous and LPS-stimulated (Bacteroides gingivalis; 5 micrograms/ml) IL-1 beta release were again significantly higher for periodontitis patients. TNF-alpha was detected in the periodontitis cultures (0-765 pg/ml per 10(6) cells), but the mean value was not significantly different from controls. LPS-stimulated TNF-alpha release, however, was significantly higher than for control subjects, and there was a strong correlation between spontaneous IL-1 beta and TNF-alpha release by monocytes from the periodontitis group. Measurement of interferon-gamma (IFN-gamma) in lymphocyte cultures from these patients by immunoradiometric assay showed that IFN-gamma levels in periodontitis cultures were consistently low, but not significantly so when compared to controls; both groups responded equally to concanavalin-A (5 micrograms/ml). Although the precise roles of IL-1 beta and TNF-alpha in periodontitis remain unclear, these data provide evidence that both cytokines may participate in the pathogenesis of the disease.