LPS-elicited secretory responses in monocytes: altered release of PGE2 but not IL-1 beta in patients with adult periodontitis.

Lipopolysaccharide responsiveness in human subjects was assessed through the examination of LPS-stimulated PGE2 and IL-1 beta release from counterflow isolated monocytes from patients with varying levels of periodontal destruction. This study was performed in order to investigate a possible relationship between LPS-mediated secretory responses in monocytes and susceptibility to periodontal destruction in humans. Subjects were chosen based on apparent resistance or susceptibility to disease as measured by little or no periodontal destruction versus generalized severe destruction, respectively. Because IFN-gamma can influence LPS-stimulated responses, the effect of IFN-gamma on the LPS-stimulated release of PGE2 and IL-1 beta was also assessed. Peripheral blood monocytes were separated by counterflow centrifugation and cultured (10(6)/ml/well) with control medium or medium containing LPS from Bacteroides gingivalis, B. intermedius, Actinobacillus actinomycetemcomitans, or Salmonella typhimurium, with or without 10 Units/ml recombinant IFN-gamma. Media were exchanged at 24 and 48 hours and culture supernatants assayed for both PGE2 and IL-1 beta by RIA. Patients classified as Susceptible to periodontitis demonstrated 2- to 3-fold greater PGE2 release than Resistant patients. This difference was observed with all LPS preparations over both the 0-24 hour and 24-48 h culture periods. IL-1 beta release, however, was not significantly different between patient groups. IFN-gamma did not affect the LPS-stimulated release of PGE2 but significantly enhanced the release of IL-1 beta. The IFN-gamma effects were similar for both patient groups. These findings indicate that LPS-stimulated PGE2 release from peripheral blood monocytes may correlate with susceptibility to periodontitis in human subjects.