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牙周细菌对生长激素释放肽受体的调节作用 及 。

Regulation of Ghrelin Receptor by Periodontal Bacteria and .

机构信息

Section of Experimental Dento-Maxillo-Facial Medicine, Center of Dento-Maxillo-Facial Medicine, University of Bonn, Bonn, Germany.

Department of Diagnosis and Surgery, School of Dentistry at Araraquara, São Paulo State University (UNESP), Araraquara, SP, Brazil.

出版信息

Mediators Inflamm. 2017;2017:4916971. doi: 10.1155/2017/4916971. Epub 2017 Nov 29.

DOI:10.1155/2017/4916971
PMID:29317796
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5727798/
Abstract

Ghrelin plays a major role in obesity-related diseases which have been shown to be associated with periodontitis. This study sought to analyze the expression of the functional receptor for ghrelin (GHS-R1a) in periodontal cells and tissues under microbial conditions and . The GHS-R1a expression in human periodontal cells challenged with the periodontopathogen , in gingival biopsies from periodontally healthy and diseased individuals, and from rats with and without ligature-induced periodontitis was analyzed by real-time PCR, immunocytochemistry, and immunofluorescence. induced an initial upregulation and subsequent downregulation of GHS-R1a in periodontal cells. In rat experimental periodontitis, the GHS-R1a expression at periodontitis sites was increased during the early stage of periodontitis, but significantly reduced afterwards, when compared with healthy sites. In human gingival biopsies, periodontally diseased sites showed a significantly lower GHS-R1a expression than the healthy sites. The expression of the functional ghrelin receptor in periodontal cells and tissues is modulated by periodontal bacteria. Due to the downregulation of the functional ghrelin receptor by long-term exposure to periodontal bacteria, the anti-inflammatory actions of ghrelin may be diminished in chronic periodontal infections, which could lead to an enhanced periodontal inflammation and tissue destruction.

摘要

胃饥饿素在与牙周炎相关的肥胖相关疾病中起主要作用。本研究旨在分析在微生物条件下和条件下，牙周细胞和组织中胃饥饿素的功能受体（GHS-R1a）的表达。通过实时 PCR、免疫细胞化学和免疫荧光分析了人牙周细胞在牙周病原体刺激下、牙周健康和患病个体的牙龈活检以及结扎诱导牙周炎大鼠中 GHS-R1a 的表达。诱导牙周细胞中 GHS-R1a 的初始上调和随后下调。在大鼠实验性牙周炎中，与健康部位相比，在牙周炎早期，牙周炎部位的 GHS-R1a 表达增加，但随后显著降低。在人类牙龈活检中，牙周病部位的 GHS-R1a 表达明显低于健康部位。牙周细胞和组织中功能性胃饥饿素受体的表达受牙周细菌调节。由于长期暴露于牙周细菌会下调功能性胃饥饿素受体，胃饥饿素的抗炎作用可能在慢性牙周感染中减弱，从而导致牙周炎症和组织破坏增强。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/144e/5727798/c493ca1bfa90/MI2017-4916971.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/144e/5727798/6ad9aff86e68/MI2017-4916971.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/144e/5727798/433df89fdd9c/MI2017-4916971.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/144e/5727798/24b2296e9a20/MI2017-4916971.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/144e/5727798/c493ca1bfa90/MI2017-4916971.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/144e/5727798/6ad9aff86e68/MI2017-4916971.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/144e/5727798/433df89fdd9c/MI2017-4916971.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/144e/5727798/24b2296e9a20/MI2017-4916971.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/144e/5727798/c493ca1bfa90/MI2017-4916971.004.jpg

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