IL-10- 592c /A多态性(rs1800872)对IL-10表达的调节与经典牙周病原体的存在和细菌载量无关

Franco Cavalla , Marcela Claudino , Elcia Varise Silveira , Andreia Espindola Vieira , Carlos Eduardo Repeke , Walter Martins Jr. , Gustavo P. Garlet
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引用次数: 1

摘要

目的探讨单核苷酸多态性(SNP) IL-10-592 C/A对牙周病原菌牙龈假单胞菌、连翘假单胞菌、齿状假单胞菌和放线菌发生及负荷的可能影响;以及微生物和遗传因素对局部IL-10 mRNA水平调节的影响。方法纳入117例病例和58例对照组。临床检查后采集微生物标本,采用RT-PCR对目的菌种进行检测/定量。采用限制性片段长度多态性(RFLP)检测SNP rs1800872。结果rs1800872的等位基因分布符合Hardy-Weinberg平衡(P = 64)。正如先前报道的那样,多态受试者表现出IL-10表达降低和患慢性牙周炎的风险增加。IL-10-592C/A rs1800872 SNP与病原菌的检测和细菌负荷无关。此外,牙周部位细菌的存在/负荷并不影响IL-10的表达,这是由研究对象的遗传背景决定的。IL-10-592C/A SNP与致病菌的检测/细菌负荷无关。IL-10的表达水平由遗传背景决定,与细菌微环境无关。
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La modulación de la expresión de IL-10 por el polimorfismo IL-10-592C/A (rs1800872) es independiente de la presencia y carga bacteriana de los periodontopatógenos clásicos

Objective

A study was conducted to investigate the possible influence of the single nucleotide polymorphism (SNP) IL-10-592 C/A on the occurrence and load of the periodontal pathogens: P. gingivalis, T. forsythia, T. denticola and A. Actinomycetemcomitans; as well to investigate the influence of microbial and genetic factors on the modulation of local IL-10 mRNA levels.

Methodology

The study included 117 cases and 58 controls. After clinical examination microbiological samples were obtained and the detection/quantification of the target bacterial species was performed by RT-PCR. SNP rs1800872 was assayed by restriction fragment length polymorphism (RFLP).

Results

Allele distribution of rs1800872 was in Hardy-Weinberg equilibrium (P = 64). As previously reported, polymorphic subjects demonstrated decreased IL-10 expression and increased risk of suffering chronic periodontitis. IL-10-592C/A rs1800872 SNP was not associated with the detection or the bacterial load of the investigated pathogens. Moreover, the presence/load of bacteria at periodontal sites did not influence IL-10 expression, which was determined by the genetic background of the study subjects. IL-10-592C/A SNP was not associated with detection/bacterial load of pathogenic bacteria. IL-10 expression levels were determined by the genetic background and were independent of the bacterial microenvironment.

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