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.
No takes yet. Share an insight, caveat, or question.
Sismey‐Durrant et al. (1991) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: