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

Abstract

Lipopolysaccharide responsiveness in human subjects was assessed through the examination of LPS-stimulated PGE₂ and IL-1/β 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-γ can influence LPS-stimulated responses, the effect of IFN-γ on the LPS-stimulated release of PGE₂ and IL-1β was also assessed. Peripheral blood monocytes were separated by counterflow centrifugation and cultured (10⁶/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-γ. Media were exchanged at 24 and 48 hours and culture supernatants assayed for both PGE, and IL-1β 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-1β release, however, was not significantly different between patient groups. IFN-γ did not affect the LPS-stimulated release of PGE₂ but significantly enhanced the release of IL-1β. The IFN-γ 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.