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.
Ferreira
Samuel B
SB
Department of Biological Sciences, School of Dentistry of Bauru, São Paulo University (FOB/USP), Bauru, SP, Brazil.
Trombone
Ana Paula F
AP
Repeke
Carlos E
CE
Cardoso
Cristina R
CR
Martins
Walter
W
Santos
Carlos F
CF
Trevilatto
Paula Cristina
PC
Avila-Campos
Mario J
MJ
Campanelli
Ana Paula
AP
Silva
João S
JS
Garlet
Gustavo P
GP
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