The Secretion of PGE₂, IL‐1β, IL‐6, and TNFα by Adherent Mononuclear Cells From Early Onset Periodontitis Patients

Abstract

The secretion of prostaglandin E2 (PGE2), tumor necrosis factor alpha (TNFα), interleukin 1 beta (IL‐1β), and interleukin 6 (IL‐6) by adherent mononuclear cells (AMNC) from 28 patients with early‐onset periodontitis was studied. The early onset‐periodontitis patients consisted of 12 patients with localized juvenile periodontitis (LJP) and 16 patients with severe generalized periodontitis (SGP). The AMNC responses to different concentrations of lipopolysaccharide (LPS) (E. coli) were determined in these 28 patients and compared to 14 healthy controls. Mediator levels in the supernatant were measured using radioimmunoassays for PGE2, IL‐1β, and IL‐6 determination and an enzyme linked immunosorbent assay for TNFα levels. The mean age of the patients was 19.9 years for the LJP group, 30.4 years for SGP, and 28.0 years for the controls. The mean number of teeth per patient with attachment loss of >6 mm was 4.75 in the LJP patients and 17.3 in the SGP group. In the absence of LPS, LJP AMNC secreted significantly more PGE2 than unstimulated control or SGP AMNC, while similar baseline amounts of IL‐1β, IL‐6, and TNFα were secreted by AMNC from the 3 patient groups. LPS stimulation resulted in the dose‐dependent secretion of significantly higher levels of PGE2 by LJP AMNC compared to SGP AMNC which in turn secreted significantly more than controls. TNFα secretion by LJP monocytes was significantly greater than the SGP and the control groups while IL‐1β secretion by the SGP AMNC was depressed compared to the other two patient groups. No significant difference in IL‐6 secretion was noted among the 3 patient groups. These data suggest that the AMNC from the peripheral blood from each of the 3 patient groups differ considerably in their capacity to secrete inflammatory mediators. It is not clear as to whether these intergroup differences in systemic AMNC responsiveness represent an intrinsic or acquired difference in LPS responsiveness. J Periodontol 1994;65:139–146.

Regulation of Immunoglobulin G2 Production by Prostaglandin E2and Platelet-Activating Factor

“…Several lines of evidence indicate that the periodontal tissues of LJP patients contain elevated amounts of PGE 2 (9,24,25). Cells of the macrophage/monocyte lineage are a major source of PGE 2 , and a recent study indicates that peripheral blood monocytes from LJP patients produce more PGE 2 than cells from periodontally healthy subjects (30). Therefore, experiments were performed to determine if IgG2 production could be enhanced by PGE 2 .…”

“…Interestingly, the myeloid cells of LJP patients are known to be somewhat abnormal. Among these abnormalities is the production of unusually large amounts of prostaglandin E 2 (PGE 2 ) by both resting and LPS-activated LJP monocytes (30). These observations prompted the hypothesis that PGE 2 could be responsible, at least in part, for the increased IgG2 production that is observed in LJP patients.…”

Factors Affecting IL-1-Mediated Collagen Metabolism By Fibroblasts and the Pathogenesis of Periodontal Disease: A Review of the Literature

“…Even lower concentrations of IL-1I: from LPS-stimulated PB monocytes from periodontitis-susceptible than from periodontitisresistant subjects have been reported (Payne et al, 1993). Further, studies have shown that the PB mononuclear cell IL-la response to oral bacterial strains did not differ among periodontitis categories (Kjeldsen et al, 1995b) and that the endogenous (unstimulated) expression of IL-13 did not differ between periodontitis and clinically healthy subjects (Shapira et al, 1994). These discrepancies, and the apparent individual variation in IL-1 production, may possibly be explained by differences in inclusion criteria for categorizing individuals, numbers of individuals, and variations in disease activity (McFarlane et al, 1990;Gemmell and Seymour, 1993 (Dower et al, 1986a;Mizel et al, 1987), and since most receptor studies have been carried out on T-cells, the following description of the fibroblast IL-I receptor will be supplemented with characteristics of the T-cell receptor.…”

Modulation of an Interleukin-12 and Gamma Interferon Synergistic Feedback Regulatory Cycle of T-Cell and Monocyte Cocultures byPorphyromonas gingivalisLipopolysaccharide in the Absence or Presence of Cysteine Proteinases

“…Isolation of human peripheral blood monocytes. Fresh monocytes were isolated from the blood of healthy donors by the adherence method (34). Briefly, PBMC were separated from healthy volunteers (Blood bank, Red Cross Transfusion Service, Sydney, New South Wales, Australia) using Ficoll-Hypaque gradients (2).…”