Quantitative gene expression profiling implicates genes for susceptibility and resistance to alveolar bone loss
Quantitative gene expression profiling implicates genes for susceptibility and resistance to alveolar bone loss
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DOI：
10.1128/iai.72.8.4471-4479.2004
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发表时间：
2004-08-01
影响因子：
3.1
通讯作者：
Baker, PJ
中科院分区：
文献类型：
--
作者：
Hart, GT;Shaffer, DJ;Baker, PJ
牙周病是最常见的慢性炎症性疾病之一。对这种疾病的易感性和抵抗力有遗传因素。使用小鼠模型，我们通过易感和耐药小鼠品系（分别为BALB/cByJ和A/J）的基因表达谱研究了牙槽骨丢失的进展。我们采用了一种新的和敏感的定量实时PCR方法比较基础的RNA转录的48个基因集在牙龈和脾脏和随后的变化，由于牙龈卟啉单胞菌口腔感染的基因表达。易感BALB/cByJ小鼠牙龈中白细胞介素-1 β（Il 1b）和肿瘤坏死因子α（Tnf）mRNA的基础表达高于耐药A/J小鼠牙龈。牙龈卟啉单胞菌感染后，BALB/cByJ小鼠牙龈Il 1b基因表达进一步增加，Stat 6基因表达开启，但A/J小鼠没有。A/J耐药小鼠牙龈中白细胞介素15（IL 15）的基础表达和脾脏中P-选择素（Selp）的基础表达均高于BALB/cByJ敏感小鼠。在耐药A/J小鼠中，感染后牙龈中没有基因的表达发生可检测的变化。这些结果表明一种分子表型，其中离散的差异表达基因组与遗传决定的易感性（IL 1b，Tnf和Stat 6）或耐药性（IL 15和Selp）牙槽骨丢失相关，从而深入了解这种复杂疾病的遗传病因。
Periodontal disease is one of the most prevalent chronic inflammatory diseases. There is a genetic component to susceptibility and resistance to this disease. Using a mouse model, we investigated the progression of alveolar bone loss by gene expression profiling of susceptible and resistant mouse strains (BALB/cByJ and A/J, respectively). We employed a novel and sensitive quantitative real-time PCR method to compare basal RNA transcription of a 48-gene set in the gingiva and the spleen and the subsequent changes in gene expression due to Porphyromonas gingivalis oral infection. Basal expression of interleukin-1 beta (Il1b) and tumor necrosis factor alpha (Tnf) mRNA was higher in the gingiva of the susceptible BALB/cByJ mice than in the gingiva of resistant A/J mice. Gingival Il1b gene expression increased further and Stat6 gene expression was turned on after P. gingivalis infection in BALB/cByJ mice but not in A/J mice. The basal expression of interleukin-15 (Il15) in the gingiva and the basal expression of p-selectin (Selp) in the spleen were higher in the resistant A/J mice than in the susceptible BALB/cByJ mice. In the resistant A/J mice the expression of no genes detectably changed in the gingiva after infection. These results suggest a molecular phenotype in which discrete sets of differentially expressed genes are associated with genetically determined susceptibility (Il1b, Tnf, and Stat6) or resistance (Il15 and Selp) to alveolar bone loss, providing insight into the genetic etiology of this complex disease.