Department of Periodontology, School of Dentistry, Aichi Gakuin University, 2-11 Suemori-dori, Chikusa-ku, Nagoya 464-8651, Japan.
Molecular Microbiology Group, Department of Tropical Infectious Diseases, Tropical Biosphere Research Center, University of the Ryukyus, 1 Senbaru, Nishihara-cho, Nakagami-gun, Nishihara 903-0213, Japan.
Int J Mol Sci. 2021 Nov 24;22(23):12704. doi: 10.3390/ijms222312704.
is an important causative organism of respiratory tract infections. Although periodontal bacteria have been shown to influence respiratory infections such as aspiration pneumonia, the synergistic effect of and , a periodontopathic bacterium, on pneumococcal infections is unclear. To investigate whether accelerates pneumococcal infections, we tested the effects of inoculating culture supernatant (PgSup) into -infected mice. Mice were intratracheally injected with and PgSup to induce pneumonia, and lung histopathological sections and the absolute number and frequency of neutrophils and macrophages in the lung were analyzed. Proinflammatory cytokine/chemokine expression was examined by qPCR and ELISA. Inflammatory cell infiltration was observed in -infected mice and and PgSup mixed-infected mice, and mixed-infected mice showed more pronounced inflammation in lung. The ratios of monocytes/macrophages and neutrophils were not significantly different between the lungs of -infected mice and those of mixed-infected mice. PgSup synergistically increased TNF-α expression/production and IL-17 production compared with infection alone. We demonstrated that PgSup enhanced inflammation in pneumonia caused by , suggesting that virulence factors produced by are involved in the exacerbation of respiratory tract infections such as aspiration pneumonia.
是呼吸道感染的重要病原体。虽然已经证明牙周细菌会影响如吸入性肺炎等呼吸道感染,但牙周病病原体和 之间的协同作用尚不清楚。为了研究 是否会加速肺炎球菌感染,我们测试了将 培养上清液(PgSup)接种到 感染小鼠中的效果。通过气管内注射 和 PgSup 来诱导肺炎,并分析肺组织病理学切片以及肺中中性粒细胞和巨噬细胞的绝对数量和频率。通过 qPCR 和 ELISA 检测促炎细胞因子/趋化因子的表达。在 感染的小鼠和 和 PgSup 混合感染的小鼠中观察到炎症细胞浸润,并且混合感染的小鼠在肺中表现出更明显的炎症。与混合感染的小鼠相比,单核细胞/巨噬细胞和中性粒细胞的比例在 感染的小鼠的肺中没有显着差异。与单独的 感染相比,PgSup 协同增加了 TNF-α 的表达/产生和 IL-17 的产生。我们证明 PgSup 增强了 引起的肺炎中的炎症,表明 产生的毒力因子参与了如吸入性肺炎等呼吸道感染的恶化。