Open Access

ARTICLE

The –308 polymorphism in the promoter region of the tumor necrosis factor-alpha (TNF-α) gene and ex vivo lipopolysaccharide-induced TNF-α expression in patients with aggressive periodontitis and/or type 1 diabetes mellitus

Claudio Pérez¹, Fermín E. González^1,2, Violeta Pavez³, Aida V. Araya⁴, Adam Aguirre¹, Andrea Cruzat^1,6, Juan Contreras-Levicoy^1,6, Andrés Dotte^1,6, Octavio Aravena¹, Lorena Salazar¹, Diego Catalán¹, Jimena Cuenca¹, Arturo Ferreira¹, Irene Schiattino⁵, Juan C. Aguillón¹

1 Disciplinary Program of Immunology, Institute of Biomedical Sciences (ICBM), Faculty of Medicine, University of Chile. Independencia 1027, Santiago, Chile
2 Dentomaxilofacial service, University of Chile Clinical Hospital, Santiago, Chile
3 Department of Conservative Odontology, Faculty of Odontology, University of Chile. Santiago, Chile
4 Endocrinology Section, Department of Medicine, University of Chile Clinical Hospital. Santiago, Chile
5 School of Public Health, Faculty of Medicine, University of Chile. Santiago, Chile
6 Medical Student

* Corresponding Author: J.C. Aguillón,

European Cytokine Network 2004, 15(4), 364-370.

Accepted 21 September 2004;

Abstract

Several single-nucleotide polymorphisms (SNPs) have been identified in the TNF-α gene promoter. The transition G→A at position –308 generates the TNF-α1 (G/G) and TNF-α2 (G/A or A/A) alleles, where the polymorphic TNF-α2 allele is associated with a high, in vitro TNF-α expression and an increased susceptibility to diverse illnesses. Here we study the association of the –308 TNF-α SNP with the susceptibility for developing aggressive periodontitis (AP), AP combined with type 1 diabetes mellitus (DM) and DM. We also explore the TNF-α capability expression and the presence of the –308 polymorphism. For this purpose we recruited 27 individuals with AP (AP+ group), 27 individuals with AP combined with DM (AP+/DM+ group), and 27 individuals with DM without signs of periodontitis upon clinical examination (DM+ group). The control group was comprised of 30 subjects. Genotyping for TNF-α promoter was performed by PCR-RFLP analysis. For TNF-α expression we used a blood culture system.

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Keywords

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