Effect of lipopolysaccharide from Porphyromonas gingivalis on prostaglandin E₂ and interleukin‐1β release from rat periosteal and human gingival fibroblasts in vitro

Abstract

Lipopolysaccharide (LPS) was extracted from Porphyromonas gingivalis (W83) by the Westphal procedure, nuclease-digested and ultracentrifuged. Fibroblasts were obtained from human gingival tissue and rat periosteum, grown to confluence then stimulated in serum-free medium with 0.1, 1.0 and 10.0 micrograms/ml LPS. The levels of prostaglandin E2 (PGE2) and interleukin-1 beta (IL-1 beta) released were measured after 2, 4 and 6 d by specific radioimmunoassays. Unstimulated gingival fibroblasts produced low levels of PGE2 (24.5 +/- 1.5 (SD) ng/ml) and IL-1 beta (0.34 +/- 0.29 ng/ml). LPS stimulated statistically significant dose-related increases in PGE2 and IL-1 beta at the concentrations of LPS tested. At 10.0 micrograms/ml, LPS-stimulated fibroblasts produced 363.5 +/- 40.3 ng/ml PGE2 and 1.81 +/- 0.1 ng/ml IL-1 beta in 6 d. These results demonstrate that LPS from P. gingivalis is capable of stimulating PGE2 and IL-1 beta release from fibroblasts. This would appear to be an additional mechanism by which LPS can induce tissue breakdown in periodontal disease.

Preventive Effects of a Kampo Medicine, Orento on Inflammatory Responses in Lipopolysaccharide Treated Human Gingival Fibroblasts

“…And HGFs produce inflammatory chemical mediators such as prostaglandin E 2 (PGE 2 ) and inflammatory cytokines such as interleukin (IL)-6 and IL-8 when HGFs were treated with LPS. [6][7][8][9] Therefore, we regard this experimental system, in which HGFs were treated with LPS, as in vitro periodontal disease model. Moreover, because HGFs sustain to produce PGE 2 10) and IL-6 and IL-8 11) in the presence of LPS, these mediators and cytokines in periodontal tissues are thought to be derived from HGFs.…”

Preventive Effects of a Kampo Medicine, Shosaikoto, on Inflammatory Responses in LPS-Treated Human Gingival Fibroblasts

“…And HGFs produce inflammatory cytokines such as interleukin (IL)-6 and IL-8 and eicosanoids such as PGE 2 when HGFs were treated with LPS. [10][11][12] Therefore, we regard this experimental system, in which HGFs were treated with LPS, as in vitro periodontal disease model. Moreover, because HGFs sustain to produce IL-6 and IL-8 in the presence of LPS, 13) we consider that the examinations of effect on HGFs, as well as monocytes and macrophages, are important in the study on periodontal disease.…”

Effects of Human Ageing on Periodontal Tissues

“…A 28-year follow-up study reported an odds ratio of 10.4 for people aged 36-50 years compared with people aged 5-15 years. While this result is comparable in magnitude with other clinically important risk factors (smoking odds ratio in the same study was 14), it corresponds to a mean increase in clinical attachment level of only 1.34 mm over 28 years 85 . This level of increased risk probably is not sufficient, alone, to cause tooth loss.…”

“…Gingival fibroblasts (GF) may be constantly affected by oral bacteria and their products, such as the lipopolysaccharides (LPS), present in their cell walls. The LPS induces GF to release some inflammatory cytokines such as prostaglandin E 2 (PGE 2 ), interleukin (IL)-1 , and plasminogen activator (PA) 6,14 . The influence of these inflammatory mediators on both GF and periodontal ligament fibroblasts (PLF) might account for the severity of periodontal disease 6 .…”