Hemoglobin and LPS act in synergy to amplify the inflammatory response
Hemoglobin and LPS act in synergy to amplify the inflammatory response
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DOI：
10.1177/154405910708600914
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发表时间：
2007-09-01
影响因子：
7.6
通讯作者：
Grenier, D.
中科院分区：
文献类型：
--
作者：
Bodet, C.;Chandad, F.;Grenier, D.
牙周炎时血管破裂和出血可能会增加龈沟液中血红蛋白的水平。本研究旨在探讨血红蛋白对牙周炎病原菌脂多糖（LPS）刺激的人巨噬细胞炎症反应的影响。通过ELISA分析在存在或不存在人血红蛋白的情况下用牙龈卟啉单胞菌和具核梭杆菌LPS攻击后巨噬细胞产生的白细胞介素-1 β（IL- 1 β）、IL- 6、IL- 8和肿瘤坏死因子α（TNF-α）。用H-3-LPS评价血红蛋白对LPS与巨噬细胞结合的影响。血红蛋白和来自牙周病原体的LPS协同作用，刺激巨噬细胞产生高水平的IL- 1 β、IL- 6、IL- 8和TNF-α。血红蛋白还增强LPS与巨噬细胞的结合。这项研究表明，血红蛋白有助于增加牙周部位的促炎介质的水平，协同作用与LPS从牙周病原体，从而有利于牙周炎的进展。
Vascular disruption and bleeding during periodontitis likely increase the levels of hemoglobin in gingival crevicular fluid. The aim of this study was to investigate the effect of hemoglobin on the inflammatory responses of human macrophages stimulated with lipopoly saccharides ( LPS) isolated from periodonto pathogens. The production of interleukin- 1 beta ( IL- 1 beta), IL- 6, IL- 8, and tumor necrosis factor alpha ( TNF- alpha) by macrophages following challenges with Porphyromonas gingivalis and Fusobacterium nucleatum LPS in the presence or absence of human hemoglobin was analyzed by ELISA. The effect of hemoglobin on LPS- binding to macrophages was evaluated with H-3-LPS. Hemoglobin and LPS from periodontopathogens acted in synergy to stimulate the production of high levels of IL- 1 beta, IL- 6, IL- 8, and TNF- alpha by macrophages. Hemoglobin also enhanced LPS-binding to macrophages. This study suggests that hemoglobin contributes to increases in the levels of pro-inflammatory mediators in periodontal sites by acting in synergy with LPS from periodonto pathogens, thus favoring the progression of periodontitis.