Polymorphisms of the interleukin-18 gene in periodontitis patients

被引:42
作者
Folwaczny, M
Glas, J
Török, HP
Tonenchi, L
Paschos, E
Bauer, B
Limbersky, O
Folwaczny, C
机构
[1] Univ Munich, Dept Operat Dent & Periodontol, Poliklin Zahnerhaltung & Parodontol, D-80336 Munich, Germany
[2] Univ Munich, Standort Innenstadtand, Med Klin & Med Poliklin, Munich, Germany
[3] Univ Munich, Standort Innenstadt, Chirurg Klin & Poliklin, Munich, Germany
关键词
destruction; immunity; inflammatory; innate; interferon-gamma (IFN-gamma); tissue;
D O I
10.1111/j.1600-051X.2005.00711.x
中图分类号
R78 [口腔科学];
学科分类号
1003 ;
摘要
Background: Interleukin (IL)-18 regulates the expression of the proinflammatory cytokine interferon (IFN)-gamma. The present study sought to test the putative involvement of six different IL-18 gene polymorphisms in pre-disposition to destructive periodontal disease. Methods: A total of 123 patients with periodontitis and 121 healthy controls were genotyped for six IL-18 polymorphisms at position -656, -607, -137, +113, +127 and codon 35/3. Genotyping has been performed by PCR and restriction fragment length polymorphism analysis. The frequencies of alleles and genotypes as well of haplotypes within both study groups were compared using the Pearson Chi-square test at a level of significance of 5% (p < 0.05). Results: Coseggregation was found to be 100% for the two polymorphisms at position -656 and -607 as well as for the polymorphisms at position -137, +113, and +127. The distribution of genotypes for the IL-18 gene polymorphism at position -656/-607 (p=0.854), at position -137/+113/+127 (p=0.320), and at codon 35/3 (p=0.481) was not significantly different among periodontitis patients if compared with healthy control subjects. The distribution of haplotype combinations for the -607 and -137 polymorphism also showed not significant difference between the both study groups (p=0.545). Conclusion: Herein the six different IL-18 gene polymorphisms were not associated with destructive periodontal disease.
引用
收藏
页码:530 / 534
页数:5
相关论文
共 26 条
[11]   Interferon-gamma deficiency attenuates local P-gingivalis induced inflammation [J].
Houri-Haddad, Y ;
Soskolne, WA ;
Shai, E ;
Palmon, A ;
Shapira, L .
JOURNAL OF DENTAL RESEARCH, 2002, 81 (06) :395-398
[12]   Association between IL-18 gene promoter polymorphisms and CTLA-4 gene 49A/G polymorphism in Japanese patients with type I diabetes [J].
Ide, A ;
Kawasaki, E ;
Abiru, N ;
Sun, F ;
Kobayashi, M ;
Fukushima, T ;
Takahashi, R ;
Kuwahara, H ;
Kita, A ;
Oshima, K ;
Uotani, S ;
Yamasaki, H ;
Yamaguchi, Y ;
Eguchi, K .
JOURNAL OF AUTOIMMUNITY, 2004, 22 (01) :73-78
[13]   Interleukin-18 promoter Polymorphisms in type 1 diabetes [J].
Kretowski, A ;
Mironczuk, K ;
Karpinska, A ;
Bojaryn, U ;
Kinalski, M ;
Puchalski, Z ;
Kinalska, I .
DIABETES, 2002, 51 (11) :3347-3349
[14]   A SIMPLE SALTING OUT PROCEDURE FOR EXTRACTING DNA FROM HUMAN NUCLEATED CELLS [J].
MILLER, SA ;
DYKES, DD ;
POLESKY, HF .
NUCLEIC ACIDS RESEARCH, 1988, 16 (03) :1215-1215
[15]   Synergy of IL-12 and IL-18 for IFN-γ gene expression:: IL-12-induced STAT4 contributes to IFN-γ promoter activation by up-regulating the binding activity of IL-18-induced activator protein 1 [J].
Nakahira, M ;
Ahn, HJ ;
Park, WR ;
Gao, P ;
Tomura, M ;
Park, CS ;
Hamaoka, T ;
Ohta, T ;
Kurimoto, M ;
Fujiwara, H .
JOURNAL OF IMMUNOLOGY, 2002, 168 (03) :1146-1153
[16]  
NYMAN S, 1997, CLIN PERIODONTOLOGY, P383
[17]   CLONING OF A NEW CYTOKINE THAT INDUCES IFN-GAMMA PRODUCTION BY T-CELLS [J].
OKAMURA, H ;
TSUTSUI, H ;
KOMATSU, T ;
YUTSUDO, M ;
HAKURA, A ;
TANIMOTO, T ;
TORIGOE, K ;
OKURA, T ;
NUKADA, Y ;
HATTORI, K ;
AKITA, K ;
NAMBA, M ;
TANABE, F ;
KONISHI, K ;
FUKUDA, S ;
KURIMOTO, M .
NATURE, 1995, 378 (6552) :88-91
[18]   Milestones in periodontal research and the remaining critical issues [J].
Page, RC .
JOURNAL OF PERIODONTAL RESEARCH, 1999, 34 (07) :331-339
[19]   Interleukin-18 (IFNγ-inducing factor) induces IL-8 and IL-1β via TNFα production from non-CD14+ human blood mononuclear cells [J].
Puren, AJ ;
Fantuzzi, G ;
Gu, Y ;
Su, MSS ;
Dinarello, CA .
JOURNAL OF CLINICAL INVESTIGATION, 1998, 101 (03) :711-721
[20]   Single-nucleotide polymorphisms of the interleukin-18 gene promoter region in rheumatoid arthritis patients: protective effect of AA genotype [J].
Sivalingam, SP ;
Yoon, KH ;
Koh, DR ;
Fong, KY .
TISSUE ANTIGENS, 2003, 62 (06) :498-504