Immunomodulation of dendritic cells differentiated in the presence of nicotine with lipopolysaccharide from Porphyromonas gingivalis.
Immunomodulation of dendritic cells differentiated in the presence of nicotine with lipopolysaccharide from Porphyromonas gingivalis.
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DOI：
10.1111/j.1600-0722.2012.00992.x
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发表时间：
2012-10
影响因子：
1.9
通讯作者：
M. Yanagita;K. Mori;R. Kobayashi;Y. Kojima;M. Kubota;K. Miki;S. Yamada;M. Kitamura;S. Murakami
中科院分区：
文献类型：
--
作者：
M. Yanagita;K. Mori;R. Kobayashi;Y. Kojima;M. Kubota;K. Miki;S. Yamada;M. Kitamura;S. Murakami
吸烟是牙周病的一个重要危险因素。尼古丁是香烟烟雾中研究最多的成分之一，被认为可以改变免疫反应。树突状细胞（Dendritic cells，DCs）是先天免疫和适应性免疫之间的关键介导者，它刺激幼稚T细胞分化为效应T细胞亚群，这些效应T细胞亚群可能积极参与牙周病的免疫发病机制。在这项研究中，我们评估了尼古丁和脂多糖（LPS）从牙龈卟啉单胞菌，单独和组合，对人单核细胞来源的DC的功能，阐明吸烟相关的牙周病的组织破坏的机制。牙龈卟啉单胞菌LPS刺激的DC与尼古丁（NiDC）分化诱导较低的T细胞增殖和人类白细胞抗原（HLA）-DR表达，但程序性细胞死亡配体1的表达升高。此外，NiDC损害了干扰素-γ的产生，但维持了共培养的T细胞中白细胞介素（IL）-5和IL-10的产生。此外，与在没有尼古丁的情况下分化的DC相比，NiDCs产生较低水平的促炎细胞因子。有趣的是，NiDCs优先产生辅助性T细胞2（Th 2）型趋化因子巨噬细胞趋化蛋白-1和巨噬细胞衍生的趋化因子。这些结果表明，在DC分化过程中尼古丁的存在调节牙龈卟啉单胞菌LPS刺激的DC的免疫调节功能。
Tobacco smoking is a significant risk factor for periodontal diseases. Nicotine, one of the most studied constituents in cigarette smoke, is thought to modify immune responses. Dendritic cells (DCs), which are key mediators between innate and adaptive immunity, stimulate naive T cells to differentiate to effector T-cell subsets that may be actively involved in the immunopathogenesis of periodontal diseases. In this study, we evaluated the effects of nicotine and lipopolysaccharide (LPS) from Porphyromonas gingivalis, alone and in combination, on the functions of human monocyte-derived DCs to elucidate the mechanism of tissue destruction of smoking-associated periodontal diseases. P. gingivalis LPS-stimulated DCs differentiated with nicotine (NiDCs) induced lower T-cell proliferation and human leukocyte antigen (HLA)-DR expression, but elevated expression of programmed cell death ligand 1. Additionally, NiDCs impaired interferon-γ production but maintained interleukin (IL)-5 and IL-10 production in co-cultured T cells. Furthermore, NiDCs produced lower levels of proinflammatory cytokines compared with DCs differentiated in the absence of nicotine. Interestingly, NiDCs preferentially produced the T helper 2 (Th2)-type chemokines macrophage chemotactic protein-1 and macrophage-derived chemokine. These results suggest that the presence of nicotine during differentiation of DCs modulates the immunoregulatory functions of P. gingivalis LPS-stimulated DCs.