Ishizuka Satoshi, Yamaya Mutsuo, Suzuki Tomoko, Takahashi Hidenori, Ida Shiroh, Sasaki Takahiko, Inoue Daisuke, Sekizawa Kiyohisa, Nishimura Hidekazu, Sasaki Hidetada
Department of Geriatric and Respiratory Medicine, Tohoku University School of Medicine, Sendai, Japan.
J Infect Dis. 2003 Dec 15;188(12):1928-39. doi: 10.1086/379833. Epub 2003 Dec 3.
To examine the effects of rhinovirus (RV) infection on the adherence of Streptococcus pneumoniae to human tracheal epithelial cells, cells were infected with RV-14, and S. pneumoniae were added to the culture medium. The number of S. pneumoniae adhering to epithelial cells increased after RV infection. Y-24180, a specific inhibitor of the platelet-activating factor receptor (PAF-R); PAF; and the pyrrolidine derivative of dithiocarbamate, an inhibitor of transcription factor nuclear factor-kappaB (NF-kappaB), decreased the number of S. pneumoniae adhering to cells after RV-14 infection. RV-14 infection increased PAF-R expression and the activation of NF-kappaB and promoter-specific transcription factor 1. These findings suggest that RV-14 infection stimulates S. pneumoniae adhesion to airway epithelial cells via increases in PAF-Rs that are partly mediated through activation of transcription factors. Increased adherence of S. pneumoniae may be one of the reasons that pneumonia develops after RV infection.
为研究鼻病毒(RV)感染对肺炎链球菌黏附人气管上皮细胞的影响,用RV - 14感染细胞,然后将肺炎链球菌添加到培养基中。RV感染后,黏附于上皮细胞的肺炎链球菌数量增加。血小板活化因子受体(PAF - R)的特异性抑制剂Y - 24180、PAF以及转录因子核因子-κB(NF -κB)的抑制剂二硫代氨基甲酸酯的吡咯烷衍生物,均可减少RV - 14感染后黏附于细胞的肺炎链球菌数量。RV - 14感染增加了PAF - R的表达以及NF -κB和启动子特异性转录因子1的激活。这些发现表明,RV - 14感染通过增加PAF - R来刺激肺炎链球菌黏附于气道上皮细胞,这部分是通过转录因子的激活介导的。肺炎链球菌黏附增加可能是RV感染后发生肺炎的原因之一。