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牙周病原菌具核梭杆菌诱导人呼吸道上皮细胞系及小鼠下呼吸道器官产生促炎细胞因子。

The Periodontopathic Bacterium Fusobacterium nucleatum Induced Proinflammatory Cytokine Production by Human Respiratory Epithelial Cell Lines and in the Lower Respiratory Organs in Mice.

作者信息

Hayata Mayumi, Watanabe Norihisa, Tamura Muneaki, Kamio Noriaki, Tanaka Hajime, Nodomi Keiko, Miya Chihiro, Nakayama Enri, Ueda Koichiro, Ogata Yorimasa, Imai Kenichi

机构信息

Department of Dysphagia Rehabilitation, Nihon University School of Dentistry, Chiyoda-ku, Tokyo, Japan.

Department of Microbiology, Nihon University School of Dentistry, Chiyoda-ku, Tokyo, Japan.

出版信息

Cell Physiol Biochem. 2019;53(1):49-61. doi: 10.33594/000000120.

Abstract

BACKGROUND/AIMS: The most prevalent infectious disease, chronic periodontitis which leads to alveolar bone destruction and subsequent tooth loss, develops due to proinflammatory cytokine production induced by periodontopathic bacteria. Chronic obstructive pulmonary disease (COPD), a non-infectious disease, is the third leading cause of death globally. This condition exacerbates frequently, and which is attributable to proinflammatory cytokine production induced by infection by respiratory microorganisms such as Streptococcus pneumoniae. Although a positive association has recently been revealed between chronic periodontitis and COPD, how periodontitis contributes to the pathogenesis of COPD remains unclear. Therefore, we hypothesized that some periodontopathic bacteria are involved in the exacerbation of COPD through the induction of proinflammatory cytokine production by respiratory epithelial cells. In this connection, COPD develops in the airways; however, because most periodontopathic bacteria are anaerobic, they are unlikely to exhibit stable virulence in the lower respiratory organs in humans. Hence, we aimed to elucidate whether exposure to heat-inactivated periodontopathic bacteria induces proinflammatory cytokine production by several human respiratory epithelial cell lines and in the lower respiratory organs and serum in mice.

METHODS

Real-time polymerase chain reaction and enzyme-linked immunosorbent assay (ELISA) were used to investigate in vitro induction by heat-inactivated periodontopathic bacteria and S. pneumoniae for mRNA expression and protein production of interleukin (IL)-8 and IL-6 by human respiratory epithelial cell lines. ELISA was also used to determine in vivo induction of cytokine production in the lower respiratory organs and serum of intratracheally heat-inactivated Fusobacterium nucleatum-inoculated mice.

RESULTS

Some, but not all, periodontopathic bacteria, especially F. nucleatum, strongly induced IL-8 and IL-6 production by BEAS-2B bronchial epithelial cells. In addition, F. nucleatum induced IL-8 production by A549 alveolar epithelial cells as well as IL-8 and IL-6 production by Detroit 562 pharyngeal epithelial cells. Furthermore, F. nucleatum induced considerably higher cytokine production than S. pneumoniae. This was also observed in the entire lower respiratory organs and serum in mice.

CONCLUSION

Exposure to increased number of F. nucleatum potentially induces proinflammatory cytokine production by human bronchial and pharyngeal epithelial cells, which may trigger exacerbation of COPD.

摘要

背景/目的:最常见的感染性疾病——慢性牙周炎会导致牙槽骨破坏并继而导致牙齿脱落,它是由牙周病原菌诱导产生促炎细胞因子而引发的。慢性阻塞性肺疾病(COPD)是一种非感染性疾病,是全球第三大死因。这种疾病频繁恶化,这归因于呼吸道微生物(如肺炎链球菌)感染诱导产生的促炎细胞因子。尽管最近已揭示慢性牙周炎与COPD之间存在正相关,但牙周炎如何促成COPD的发病机制仍不清楚。因此,我们推测一些牙周病原菌通过诱导呼吸道上皮细胞产生促炎细胞因子而参与COPD的恶化。就此而言,COPD在气道中发展;然而,由于大多数牙周病原菌是厌氧菌,它们不太可能在人类下呼吸道器官中表现出稳定的毒力。因此,我们旨在阐明暴露于热灭活的牙周病原菌是否会诱导几种人呼吸道上皮细胞系以及小鼠下呼吸道器官和血清产生促炎细胞因子。

方法

采用实时聚合酶链反应和酶联免疫吸附测定(ELISA)来研究热灭活的牙周病原菌和肺炎链球菌对人呼吸道上皮细胞系白细胞介素(IL)-8和IL-6的mRNA表达和蛋白质产生的体外诱导作用。ELISA还用于测定气管内接种热灭活具核梭杆菌的小鼠下呼吸道器官和血清中细胞因子产生的体内诱导情况。

结果

一些但并非所有的牙周病原菌,尤其是具核梭杆菌,能强烈诱导BEAS-2B支气管上皮细胞产生IL-8和IL-6。此外,具核梭杆菌诱导A549肺泡上皮细胞产生IL-8以及底特律562咽上皮细胞产生IL-8和IL-6。此外,具核梭杆菌诱导产生的细胞因子比肺炎链球菌高得多。在小鼠的整个下呼吸道器官和血清中也观察到了这一点。

结论

暴露于数量增加的具核梭杆菌可能会诱导人支气管和咽上皮细胞产生促炎细胞因子,这可能会引发COPD的恶化。

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