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伴放线放线杆菌脂多糖与微小消化链球菌的结合可刺激巨噬细胞样细胞产生肿瘤坏死因子α。

Binding of Actinobacillus actinomycetemcomitans lipopolysaccharides to Peptostreptococcus micros stimulates tumor necrosis factor alpha production by macrophage-like cells.

作者信息

Yoshioka M, Grenier D, Mayrand D

机构信息

Department of Preventive Dentistry, School of Dentistry, University of Tokushima, Tokushima, Japan.

出版信息

Oral Microbiol Immunol. 2005 Apr;20(2):118-21. doi: 10.1111/j.1399-302X.2004.00204.x.

Abstract

Peptostreptococcus micros is a gram-positive bacterium that has been associated with periodontitis and endodontic infections. In this study, we hypothesized that P. micros binds the immunomodulating component lipopolysaccharide derived from gram-negative bacteria to increase its capacity to stimulate cytokine production by host cells. The ability of P. micros to bind Actinobacillus actinomycetemcomitans lipopolysaccharide was demonstrated by an enzyme-linked immunosorbent assay and by immunoelectron microscopy. Pretreatment of P. micros cells with A. actinomycetemcomitans lipopolysaccharide was associated with a 49-fold increase in tumor necrosis factor alpha production by human monocytic cells U937 differentiated into adherent macrophages, compared to the stimulation with untreated P. micros. This effect was suppressed by incorporating polymyxin B, a lipid A-binding substance, during treatment of macrophage-like cells with lipopolysaccharide-coated P. micros cells. This is the first study reporting a binding interaction between lipopolysaccharide and a gram-positive bacterium. This interaction represents a new mechanism that could promote the inflammatory response during periodontitis.

摘要

微小消化链球菌是一种革兰氏阳性菌,与牙周炎和牙髓感染有关。在本研究中,我们假设微小消化链球菌结合源自革兰氏阴性菌的免疫调节成分脂多糖,以增加其刺激宿主细胞产生细胞因子的能力。通过酶联免疫吸附测定和免疫电子显微镜证实了微小消化链球菌结合伴放线放线杆菌脂多糖的能力。与未处理的微小消化链球菌刺激相比,用伴放线放线杆菌脂多糖预处理微小消化链球菌细胞后,分化为贴壁巨噬细胞的人单核细胞U937产生的肿瘤坏死因子α增加了49倍。在用脂多糖包被的微小消化链球菌细胞处理巨噬样细胞的过程中加入多粘菌素B(一种脂质A结合物质)可抑制这种效应。这是第一项报道脂多糖与革兰氏阳性菌之间存在结合相互作用的研究。这种相互作用代表了一种可能促进牙周炎炎症反应的新机制。

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