Peptostreptococcus micros cell wall elicits a pro-inflammatory response in human macrophages.

Shin-ichi Tanabe, Charles Bodet, Daniel Grenier
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引用次数: 39

Abstract

Peptostreptococcus micros is a Gram-positive anaerobic bacterium associated with periodontitis, a chronic inflammatory disease affecting tooth-supporting tissues. In the present study, we investigated the response of human macrophages to stimulation with a cell wall preparation from P. micros. In addition, the effect of the preparation on the phosphorylation of macrophage kinases was studied. The preparation, which was non-toxic for macrophages, significantly increased the secretion of the pro-inflammatory cytokines TNF-alpha, IL-1beta and IL-6. It also increased the secretion of two potent chemokines IL-8 and, to a lesser extent, RANTES. Lastly, stimulation of macrophages by the P. micros cell wall preparation induced a significant increase in MMP-9 secretion but had no effect on the production of prostaglandin E2. The phosphorylation of macrophage kinases, including cAMP-dependent protein-serine kinase (PKA) catalytic subunit beta, G protein-coupled receptor-serine kinase 2, mitogen-activated protein-serine kinase p38 alpha (p38a MAPK), extracellular regulated protein-serine kinase 2 (ERK2) and Jun N-terminus protein-serine kinases (JNK), increased following stimulation with cell wall. In summary, our study showed that the P. micros cell wall preparation induced intracellular signaling pathways, leading to an increased production of pro-inflammatory cytokines, chemokines and MMP-9 by macrophages.

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微胃链球菌细胞壁引起人巨噬细胞的促炎反应。
微胃链球菌是一种与牙周炎相关的革兰氏阳性厌氧菌,牙周炎是一种影响牙齿支撑组织的慢性炎症性疾病。在本研究中,我们研究了人巨噬细胞对刺激的反应。此外,还研究了该制剂对巨噬细胞激酶磷酸化的影响。该制剂对巨噬细胞无毒,可显著增加促炎细胞因子tnf - α、il -1 β和IL-6的分泌。它还增加了两种有效的趋化因子IL-8的分泌,并在较小程度上增加了RANTES的分泌。最后,通过P. micros细胞壁制剂刺激巨噬细胞,诱导MMP-9分泌显著增加,但对前列腺素E2的产生没有影响。巨噬细胞激酶的磷酸化,包括camp依赖性蛋白-丝氨酸激酶(PKA)催化亚基β、G蛋白偶联受体-丝氨酸激酶2、丝裂原活化蛋白-丝氨酸激酶p38 α (p38a MAPK)、细胞外调节蛋白-丝氨酸激酶2 (ERK2)和Jun n端蛋白-丝氨酸激酶(JNK),在细胞壁刺激后增加。总之,我们的研究表明,P. micros细胞壁制备诱导了细胞内信号通路,导致巨噬细胞产生促炎细胞因子、趋化因子和MMP-9。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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