THE SECRETION OF PGE(2), IL-1-BETA, IL-6, AND TNF-ALPHA BY ADHERENT MONONUCLEAR-CELLS FROM EARLY-ONSET PERIODONTITIS PATIENTS

Citation
L. Shapira et al., THE SECRETION OF PGE(2), IL-1-BETA, IL-6, AND TNF-ALPHA BY ADHERENT MONONUCLEAR-CELLS FROM EARLY-ONSET PERIODONTITIS PATIENTS, Journal of periodontology, 65(2), 1994, pp. 139-146
Citations number
48
Categorie Soggetti
Dentistry,Oral Surgery & Medicine
Journal title
ISSN journal
00223492
Volume
65
Issue
2
Year of publication
1994
Pages
139 - 146
Database
ISI
SICI code
0022-3492(1994)65:2<139:TSOPII>2.0.ZU;2-8
Abstract
THE SECRETION OF PROSTAGLANDIN E(2) (PGE(2)), tumor necrosis factor al pha (TNF(alpha), interleukin 1 beta (IL-1 beta), and interleukin 6 (IL -6) by adherent mononuclear cells (AMNC) from 28 patients with early-o nset 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 radio immunoassays for PGE(2), IL-1 beta, and IL-6 determination and an enzy me linked immunosorbent assay for TNF alpha levels. The mean age of th e patients was 19.9 years for the LJP group, 30.4 years for SGP, and 2 8.0 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 PGE(2) than unstimulated control or SGP AMNC, while similar baseline amounts of IL-1 beta, IL-6, and TNF alpha were secreted by AMNC from t he 3 patient groups. LPS stimulation resulted in the dose-dependent se cretion of significantly higher levels of PGE, by LJP AMNC compared to SGP AMNC which in turn secreted significantly more than controls. TNF alpha Secretion by WP monocytes was significantly greater than the SG P and the control groups while IL-1 beta secretion by the SGP AMNC was depressed compared to the other two patient groups. No significant di fference 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 inf lammatory mediators. It is not clear as to whether these intergroup di fferences in systemic AMNC responsiveness represent an intrinsic or ac quired difference in LPS responsiveness.