John Libbey Eurotext

European Cytokine Network


Ex vivo lipopolysaccharide (LPS)‐induced TNF‐α, IL‐1β, IL‐6 and PGE 2 secretion in whole blood from Type 1 diabetes mellitus patients with or without aggressive periodontitis Volume 14, numéro 3, July 2003

Endocrinology Section, Department of Medicine, University of Chile Clinical Hospital. Santiago. Chile Department of Conservative Odontology, Faculty of Odontology, University of Chile. Santiago, Chile Disciplinary Program of Immunology, Institute of Biomedical Sciences (ICBM), Faculty of Medicine, University of Chile. Santiago, Chile School of Public Health, Faculty of Medicine, University of Chile, Santiago, Chile

Several studies have demonstrated that diabetes is a risk factor for developing periodontal disease, increasing its prevalence and severity. Furthermore, periodontitis may impair the metabolic control and adequate treatment of diabetic patients. LPS from Gram‐negative bacteria penetrates the periodontal tissues and subsequently recruits and activates immune cells. Progression to severe periodontitis with loss of supporting structures is mediated by several factors, including secretion of a broad spectrum of inflammatory and destructive mediators such as cytokines (TNF‐α, IL‐1β and IL‐6), chemokines (IL‐8) and prostaglandin E 2 (PGE 2). The aim of this work is to investigate differences in the TNF‐α, IL‐1β and IL‐6 expression and prostaglandin E 2 (PGE 2) release in blood from diabetic patients with and without aggressive periodontitis (AP) stimulated with lipopolysaccharide (LPS). For this purpose we recruited 29 Type 1 diabetes mellitus (DM) patients, 14 with AP and 15 without AP. Fourteen healthy individuals formed the control group. For cytokine expression and PGE 2 secretion, an ex vivo whole blood culture system was used . Cytokines and PGE 2 were detected by commercial immunometric assays. A wide range of inter‐individual variability in spontaneous and LPS‐induced TNF‐α, IL‐1β and IL‐6 levels in patient groups and controls was found. The mean of spontaneous and LPS‐induced TNF‐α and IL‐1β levels did not differ significantly (p > 0.5) when patients were compared to control individuals. Although not significant, the spontaneous TNF‐α, IL‐1β and IL‐6 levels in the group of Type 1 DM with AP were higher than in controls, while in diabetic patients without AP, these values were depressed in comparison with controls. In both groups of patients, the means of LPS‐induced IL‐6 levels were higher than the controls but the differences observed were not significant (p ∓ 0.07). However, the LPS‐induced PGE 2 levels varied significantly when all groups were compared (p ∓ 0.007). The means of LPS‐induced PGE 2 levels for Type 1 diabetic patients with AP (p ∓ 0.0009) and without AP (p ∓ 0.024) were significantly higher than the levels observed for healthy controls. Finally, we conclude that Type 1 diabetic patients with or without AP did not express higher LPS‐induced TNF‐α, IL‐1β and IL‐6 levels than controls. However, the PGE 2 levels released were significantly higher than those detected in controls.