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单核细胞对复杂生物膜的细胞因子反应模式可区分患者的疾病状态和生物膜生态失调。

Cytokine response patterns to complex biofilms by mononuclear cells discriminate patient disease status and biofilm dysbiosis.

作者信息

Velsko I M, Cruz-Almeida Y, Huang H, Wallet S M, Shaddox L M

机构信息

Department of Periodontology, College of Dentistry, University of Florida, Gainesville, FL, USA.

Institute for Aging, College of Medicine, University of Florida, Gainesville, FL, USA.

出版信息

J Oral Microbiol. 2017 Jun 12;9(1):1330645. doi: 10.1080/20002297.2017.1330645. eCollection 2017.

Abstract

Localized aggressive periodontitis (LAP) is a rare form of periodontal disease with site-specific rapid tissue destruction. A lipopolysaccharide (LPS) hyper-inflammatory response was shown in LAP using peripheral whole blood, although responses to other bacterial surface components or complex oral biofilms have not been evaluated. Peripheral blood mononuclear cells (PBMCs) from 14 LAP patients, 15 healthy siblings (HS), and 13 unrelated healthy controls (HC) were stimulated with: LPS, lipoteichoic acid, or peptidoglycan; intact or sonically dispersed -grown biofilms from a LAP disease site, a LAP healthy site, or a healthy control site. Cell culture supernatants were assayed for 14 cyto/chemokines. Discriminant function analysis determined cyto/chemokines that discriminate disease status by response patterns to different stimuli. Qualitative differences in the cytokine response pattern among patient groups were observed to intact and dispersed biofilms, yet responses to healthy and diseased biofilms could not be discriminated. Despite an equivalent magnitude of response, LAP-derived PBMCs demonstrated a qualitatively different pattern of response to LPS and dispersed biofilms. PMBCs from each group responded distinctly to stimulation withsubgingival biofilms. Multiple underlying mechanisms related to bacterial-induced inflammatory responses can culminate in LAP disease initiation and/or progression, and biofilm homeostasis could play an important role.

摘要

局限性侵袭性牙周炎(LAP)是一种罕见的牙周疾病形式,具有特定部位的快速组织破坏。使用外周全血研究发现,LAP患者存在脂多糖(LPS)超炎症反应,不过对其他细菌表面成分或复杂口腔生物膜的反应尚未评估。分别用LPS、脂磷壁酸或肽聚糖;来自LAP病损部位、LAP健康部位或健康对照部位的完整或经超声分散培养的生物膜,刺激14例LAP患者、15例健康同胞(HS)和13例无关健康对照(HC)的外周血单核细胞(PBMC)。检测细胞培养上清液中的14种细胞因子/趋化因子。判别函数分析确定了通过对不同刺激的反应模式来区分疾病状态的细胞因子/趋化因子。观察到患者组对完整和分散生物膜的细胞因子反应模式存在定性差异,但无法区分对健康和患病生物膜的反应。尽管反应程度相当,但源自LAP的PBMC对LPS和分散生物膜的反应模式在性质上有所不同。每组的PMBC对龈下生物膜刺激的反应各不相同。多种与细菌诱导的炎症反应相关的潜在机制可能共同导致LAP疾病的发生和/或进展,生物膜稳态可能起重要作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1df9/5508357/a312efd62364/zjom_a_1330645_f0001_c.jpg

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