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Infection and Immunity, August 2008, p. 3725-3734, Vol. 76, No. 8
0019-9567/08/$08.00+0     doi:10.1128/IAI.00546-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

An Interleukin-1β (IL-1β) Single-Nucleotide Polymorphism at Position 3954 and Red Complex Periodontopathogens Independently and Additively Modulate the Levels of IL-1β in Diseased Periodontal Tissues{triangledown}

Samuel B. Ferreira Jr.,1 Ana Paula F. Trombone,2 Carlos E. Repeke,1 Cristina R. Cardoso,2 Walter Martins Jr.,3 Carlos F. Santos,1 Paula Cristina Trevilatto,4 Mario J. Ávila-Campos,5 Ana Paula Campanelli,1 João S. Silva,2 and Gustavo P. Garlet1*

Department of Biological Sciences, School of Dentistry of Bauru, São Paulo University (FOB/USP), Bauru, SP, Brazil,1 Department of Biochemistry and Immunology, School of Medicine of Ribeirão Preto, São Paulo University (FMRP/USP), Ribeirão Preto, SP, Brazil,2 Department of Periodontics, Dentistry School of the University of Ribeirão Preto (UNAERP), Ribeirão Preto, SP, Brazil,3 School of Dentistry, Pontifical Catholic University of Paraná (PUC-PR), Curitiba, PR, Brazil,4 Department of Microbiology, Institute of Biomedical Sciences (ICB/USP), São Paulo, SP, Brazil5

Received 5 May 2008/ Returned for modification 23 May 2008/ Accepted 28 May 2008

Inflammatory cytokines such as interleukin-1β (IL-1β) are involved in the pathogenesis of periodontal diseases. A high individual variation in the levels of IL-1β 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-1β promoter single-nucleotide polymorphism at position 3954 [IL-1β(3954) SNP] and the presence of the periodontopathogens in the determination of the IL-1β 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-1β(3954) SNP was investigated by restriction fragment length polymorphism, while the IL-1β levels and the presence of the periodontopathogens were determined by real-time PCR. Similar frequencies of IL-1β(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-1β(3954) SNP CT and TT genotypes, as well as P. gingivalis, T. forsythia, and T. denticola, were associated with higher IL-1β levels and with higher values of the clinical parameters of disease severity. Concomitant analyses demonstrate that IL-1β(3954) and the red complex periodontopathogens were found to independently and additively modulate the levels of IL-1β in periodontal tissues. Similarly, the concurrent presence of both factors was associated with increased scores of disease severity. IL-1β(3954) genotypes and red complex periodontopathogens, individually and additively, modulate the levels of IL-1β in the diseased tissues of nonsmoking CP patients and, consequently, are potentially involved in the determination of the disease outcome.


* Corresponding author. Mailing address: School of Dentistry of Bauru (FOB/USP), Department of Biological Sciences, Al. Octávio Pinheiro Brisola, 9-75, CEP 17012-901, Bauru, SP, Brazil. Phone: 55 (14) 3235-8274. Fax: 55 (14) 3235-8274. E-mail: garletgp{at}usp.br

{triangledown} Published ahead of print on 9 June 2008.

Editor: A. J. Bäumler


Infection and Immunity, August 2008, p. 3725-3734, Vol. 76, No. 8
0019-9567/08/$08.00+0     doi:10.1128/IAI.00546-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.




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