Open Access

ARTICLE

Ex vivo lipopolysaccharide (LPS)-induced TNF-α, IL-1β, IL-6 and PGE₂ secretion in whole blood from Type 1 diabetes mellitus patients with or without aggressive periodontitis

A. Veronica Araya¹, Violeta Pavez², Claudio Perez³, Fermin Gonzalez³, Alicia Colombo³, Adam Aguirre³, Irene Schiattino⁴, Juan C. Aguillón³

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

* Corresponding Author: Juan C. Aguillón,

European Cytokine Network 2003, 14(3), 128-133.

Abstract

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 E₂ (PGE₂).
The aim of this work is to investigate differences in the TNF-α, IL-1β and IL-6 expression and prostaglandin E₂ (PGE₂) 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 PGE₂ secretion, an ex vivo whole blood culture system was used . Cytokines and PGE₂ 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 PGE₂ levels varied significantly when all groups were compared (p = 0.007). The means of LPS-induced PGE₂ 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 PGE₂ levels released were significantly higher than those detected in controls.

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