Differential Induction of Human Beta‐Defensin Expression by Periodontal Commensals and Pathogens in Periodontal Pocket Epithelial Cells

Vankeerberghen, Anne; Nuytten, Hilde; Dierickx, Kurt; Quirynen, Marc; Cassiman, Jean‐Jacques; Cuppens, Harry

doi:10.1902/jop.2005.76.8.1293

Cited by 76 publications

(92 citation statements)

References 38 publications

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“…The expression of hBD-1 is induced by cytokines under physiologic conditions of inflammation, and its increased secretion serves an antimicrobial host-defense function at these critical interfaces between host and environment (14). The h-defensins are part of the innate immune system and are chemotactic attractants for antigen-presenting dendritic cells, an effect that is mediated by specific cell surface receptors found on these antigen-presenting cells (15).…”

Section: Discussionmentioning

confidence: 99%

Human β-Defensin-1, a Potential Chromosome 8p Tumor Suppressor: Control of Transcription and Induction of Apoptosis in Renal Cell Carcinoma

Sun¹,

et al. 2006

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Human b-defensin-1 (hBD-1) is a candidate tumor suppressor gene located on chromosome 8p23. Previously, we showed that cancer-specific loss of hBD-1 was found in 90% of renal clear cell carcinomas and in 82% of prostate cancers. To investigate the possible mechanisms of decreased gene expression and determine the function of hBD-1 protein in urological cancers, we sequenced hBD-1 gene coding regions in prostatic and renal cancer samples. We then analyzed the frequency distribution of promoter polymorphisms and determined the effect of these base changes on transcriptional activity of the hBD-1 promoter. A polymorphism at À688 bases upstream of the ATG start codon affects hBD-1 promoter activity, leading to a rate of reporter gene transcription that is 40% to 50% lower than the wild-type sequence when tested in either DU145 or TSU-Pr1 cell lines. In addition, a polymorphism at À44 bases was shown to enhance transcription up to 2.3 times more than the wild-type sequence in the same cell lines. In addition, three novel hBD-1 promoter mutations were found in renal and prostate cancer clinical samples. An iso-5-aza-2 ¶-deoxycytidine treatment was effective in transcription up-regulation in DU145, suggesting a possible upstream methylation-dependent effect. Synthetic hBD-1 peptide inhibited bladder cancer cell TSU-Pr1 proliferation. Overexpression of the hBD-1 gene in renal cancer cells SW156 resulted in caspase-3-mediated apoptosis. These data support the hypothesis that hBD-1 is a potential tumor suppressor gene for urological cancers. Promoter point mutations may be responsible for cancer-specific loss of hDB-1 expression.

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Section: Discussionmentioning

confidence: 99%

Human β-Defensin-1, a Potential Chromosome 8p Tumor Suppressor: Control of Transcription and Induction of Apoptosis in Renal Cell Carcinoma

Sun¹,

et al. 2006

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“…The influence of oral bacteria on the expression of HBDs by gingival epithelial cells has been studied extensively in vitro. Components from several species of oral bacteria, including Streptococcus gordonii, Fusobacterium nucleatum, and Porphyromonas gingivalis, have been shown to induce HBD-2 expression (2,20,28,31); in addition, infection of oral epithelial cells with live Aggregatibacter actinomycetemcomitans induces HBD-3 (9). Previously, we reported that infection by F. nucleatum or Prevotella intermedia strongly induced the expression of both HBD-2 and -3 by gingival epithelial cells (13).…”

mentioning

confidence: 91%

Toll-Like Receptor 2 and NALP2 Mediate Induction of Human Beta-Defensins byFusobacterium nucleatumin Gingival Epithelial Cells

Ji¹,

Shin²,

Kim³

et al. 2009

Infect Immun

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“…11 It is inducible only by commensal bacteria and not, unlike hBD-2 and DEFB103, by pathogenic bacteria. 12 Therefore, DEFB1 has been suggested to be responsible for maintaining a healthy status in mucosal epithelials before infection with pathogenic bacteria, and can thus be considered to function as a guardian in the maintenance of mucosal and oral health.…”

Section: Introductionmentioning

confidence: 99%

A 3′ UTR transition within DEFB1 is associated with chronic and aggressive periodontitis

Schäefer¹,

Richter²,

Nothnagel³

et al. 2009

Genes Immun

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Periodontal diseases are complex inflammatory diseases and affect up to 20% of the worldwide population. An unbalanced reaction of the immune system toward microbial pathogens is considered as the key factor in the development of periodontitis. Defensins have a strong antimicrobial function and are important contributors of the immune system toward maintaining health. Here, we present the first systematic association study of DEFB1. Using a haplotype-tagging single nucleotide polymorphism (SNP) approach, including described promoter SNPs of DEFB1, we investigated the associations of the selected variants in a large population (N ¼ 1337 cases and 2887 ethnically matched controls). The 3 0 untranslated region SNP, rs1047031, showed the most significant association signal for homozygous carriers of the rare A allele (P ¼ 0.002) with an increased genetic risk of 1.3 (95% confidence interval: 1.11-1.57). The association was consistent with the specific periodontitis forms: chronic periodontitis (odds ratio ¼ 2.2 (95% confidence interval: 1.16-4.35), P ¼ 0.02), and aggressive periodontitis (odds ratio ¼ 1.3 (95% confidence interval 1.04-1.68), P ¼ 0.02). Sequencing of regulatory and exonic regions of DEFB1 identified no other associated variant, pointing toward rs1047031 as likely being the causative variant. Prediction of microRNA targets identified a potential microRNA-binding site at the position of rs1047031.

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Differential Induction of Human Beta‐Defensin Expression by Periodontal Commensals and Pathogens in Periodontal Pocket Epithelial Cells

Abstract: The results suggest that a correlation can be found in diseased oral epithelium between the defensin profiles that are induced and the pathogenicity of the oral bacterial strains.

Cited by 76 publications

References 38 publications

Human β-Defensin-1, a Potential Chromosome 8p Tumor Suppressor: Control of Transcription and Induction of Apoptosis in Renal Cell Carcinoma

Human β-Defensin-1, a Potential Chromosome 8p Tumor Suppressor: Control of Transcription and Induction of Apoptosis in Renal Cell Carcinoma

Toll-Like Receptor 2 and NALP2 Mediate Induction of Human Beta-Defensins byFusobacterium nucleatumin Gingival Epithelial Cells

A 3′ UTR transition within DEFB1 is associated with chronic and aggressive periodontitis

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