Correlation of Aggregatibacter actinomycetemcomitans detection with clinical/immunoinflammatory profile of localized aggressive periodontitis using a 16S rRNA microarray method: a cross-sectional study.

Correlation of Aggregatibacter actinomycetemcomitans detection with clinical/immunoinflammatory profile of localized aggressive periodontitis using a 16S rRNA microarray method: a cross-sectional study.
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DOI:
10.1371/journal.pone.0085066
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发表时间:
2013
期刊:
影响因子:
3.7
通讯作者:
Shaddox LM
Shaddox LM
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Gonçalves PF;Klepac-Ceraj V;Huang H;Paster BJ;Aukhil I;Wallet SM;Shaddox LM

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本研究的目的是确定放线菌伴聚合杆菌(Aa)的检测是否与局部侵袭性牙周炎(牙周炎)的临床和免疫炎症特征相关,通过16 S rRNA基因芯片确定。 采用16 SrRNA基因芯片对30例牙周炎患者(PD ≥ 5 mm,BoP和骨质丢失)的龈下菌斑进行分析。分析了牙龈沟液(GCF)样本中的14种细胞因子/趋化因子。获得外周血并在体外用牙龈卟啉单胞菌和大肠杆菌刺激以评估炎症反应谱。还测量了血浆脂多糖(LPS)水平。 Aa在56%的COPD患者中被检测到,并且被证明是不同细菌群落结构的指示剂(p<0.01)。在检测到Aa和未检测到Aa的组中,在LPS刺激的血液样品中检测到促炎细胞/趋化因子水平升高(p>0.05)。两组的临床参数和血清LPS水平相似。然而,未检测到Aa的GCF比检测到Aa的位点含有更高浓度的IL-8(p<0.05)。大肠杆菌LPS刺激Aa阳性患者外周血细胞后,TNFα和IL 1 β水平升高。 我们的研究结果表明,在本横断面研究中,在牙周病受累部位检测到Aa与采样时疾病的临床严重程度无关,尽管它确实与局部IL-8水平较低、龈下细菌谱不同以及LPS诱导的TNFα和IL 1 β水平升高相关。
The objective of this study was to determine whether the detection of Aggregatibacter actinomycetemcomitans (Aa) correlates with the clinical and immunoinflammatory profile of Localized Aggressive Periodontitis (LAP), as determined by by 16S rRNA gene-based microarray. Subgingival plaque samples from the deepest diseased site of 30 LAP patients [PD ≥ 5 mm, BoP and bone loss] were analyzed by 16S rRNA gene-based microarrays. Gingival crevicular fluid (GCF) samples were analyzed for 14 cyto/chemokines. Peripheral blood was obtained and stimulated in vitro with P.gingivalis and E.coli to evaluate inflammatory response profiles. Plasma lipopolysaccharide (LPS) levels were also measured. Aa was detected in 56% of LAP patients and was shown to be an indicator for different bacterial community structures (p<0.01). Elevated levels of pro-inflammatory cyto/chemokines were detected in LPS-stimulated blood samples in both Aa-detected and Aa-non-detected groups (p>0.05). Clinical parameters and serum LPS levels were similar between groups. However, Aa-non-detected GCF contained higher concentration of IL-8 than Aa-detected sites (p<0.05). TNFα and IL1β were elevated upon E.coli LPS stimulation of peripheral blood cells derived from patients with Aa-detected sites. Our findings demonstrate that the detection of Aa in LAP affected sites, did not correlate with clinical severity of the disease at the time of sampling in this cross-sectional study, although it did associate with lower local levels of IL-8, a different subgingival bacterial profile and elevated LPS-induced levels of TNFα and IL1β.
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