An interleukin-1beta (IL-1beta) single-nucleotide polymorphism at position 3954 and red complex periodontopathogens independently and additively modulate the levels of IL-1beta in diseased periodontal tissues.
Inflammatory cytokines such as interleukin-1beta (IL-1beta) are involved in the pathogenesis of periodontal diseases. A high individual variation in the levels of IL-1beta mRNA has been verified, which is possibly determined by genetic polymorphisms and/or by the presence of periodontopathogens such as Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola, and Aggregatibacter actinomycetemcomitans. In this study, we investigated the role of an IL-1beta promoter single-nucleotide polymorphism at position 3954 [IL-1beta(3954) SNP] and the presence of the periodontopathogens in the determination of the IL-1beta levels in the periodontal tissues of nonsmoking chronic periodontitis (CP) patients (n = 117) and control (C) subjects (n = 175) and the possible correlations with the clinical parameters of the disease. IL-1beta(3954) SNP was investigated by restriction fragment length polymorphism, while the IL-1beta levels and the presence of the periodontopathogens were determined by real-time PCR. Similar frequencies of IL-1beta(3954) SNP were found in the C and CP groups, in spite of a trend toward a higher incidence of T alleles in the CP group. The IL-1beta(3954) SNP CT and TT genotypes, as well as P. gingivalis, T. forsythia, and T. denticola, were associated with higher IL-1beta levels and with higher values of the clinical parameters of disease severity. Concomitant analyses demonstrate that IL-1beta(3954) and the red complex periodontopathogens were found to independently and additively modulate the levels of IL-1beta in periodontal tissues. Similarly, the concurrent presence of both factors was associated with increased scores of disease severity. IL-1beta(3954) genotypes and red complex periodontopathogens, individually and additively, modulate the levels of IL-1beta in the diseased tissues of nonsmoking CP patients and, consequently, are potentially involved in the determination of the disease outcome.
Department of Biological Sciences, School of Dentistry of Bauru, São Paulo University (FOB/USP), Bauru, SP, Brazil.
Samuel B
SB
Ferreira
Ana Paula F
AP
Trombone
Carlos E
CE
Repeke
Cristina R
CR
Cardoso
Walter
W
Martins
Carlos F
CF
Santos
Paula Cristina
PC
Trevilatto
Mario J
MJ
Avila-Campos
Ana Paula
AP
Campanelli
João S
JS
Silva
Gustavo P
GP
Garlet
D000328:Adult; D017931:DNA Primers / Q000235:genetics; D005260:Female; D005787:Gene Frequency; D005838:Genotype; D006089:Gram-Negative Anaerobic Bacteria / Q000276:immunology* / Q000302:isolation & purification; D006801:Humans; D053583:Interleukin-1beta / Q000096:biosynthesis* / Q000235:genetics; D008297:Male; D008875:Middle Aged; D010518:Periodontitis / Q000276:immunology* / Q000382:microbiology; D016133:Polymerase Chain Reaction / Q000379:methods; D012150:Polymorphism, Restriction Fragment Length; D020641:Polymorphism, Single Nucleotide; D012720:Severity of Illness Index
D017931:DNA Primers; D053583:Interleukin-1beta