Chen Hong-Yi, Lin Mei-Hui, Chen Chien-Cheng, Shu Jwu-Ching
Department of Medical Biotechnology and Laboratory Science, College of Medicine, Chang Gung University, No. 259, Wenhua 1st Road, Guishan, Taoyuan, 333, Taiwan.
Research Center for Pathogenic Bacteria, Chang Gung University, Taoyuan, Taiwan.
BMC Microbiol. 2017 Apr 13;17(1):92. doi: 10.1186/s12866-017-1003-9.
Fibronectin (Fn) plays a major role in the attachment of Staphylococcus aureus to host cells by bridging staphylococcal fibronectin-binding proteins (FnBPs) and cell-surface integrins. A previous study demonstrated that the phagocytosis of S. aureus by macrophages is enhanced in the presence of exogenous Fn. We recently found that FnBPs overexpression also enhances phagocytic activity. The effect of S. aureus infection on the expression of macrophage Fn was investigated.
The level of Fn secreted by monocytes (THP-1), macrophages, human lung adenocarcinoma (A549) cells, and hepatocellular carcinoma (HepG2) cells in response to S. aureus infection was determined by Western blotting and it was significantly suppressed only in macrophages. The activation of signaling pathways associated with Fn regulation in macrophages and HepG2 cells was also investigated by Western blotting. Erk was activated in both macrophages and HepG2 cells, whereas Src-JNK-c-Jun signaling was only activated in macrophages. A significant decrease in macrophage viability was observed in response to S. aureus infection in the presence of exogenous Fn.
The Src-JNK-c-Jun signaling pathway was activated in macrophages in response to S. aureus infection and resulted in the suppression of Fn expression. This suppression may play a protective role in macrophages against S. aureus infection. This study provides the first demonstration that Fn is suppressed in macrophages by S. aureus infection.
纤连蛋白（Fn）通过连接葡萄球菌纤连蛋白结合蛋白（FnBPs）和细胞表面整合素，在金黄色葡萄球菌附着于宿主细胞的过程中发挥主要作用。先前的一项研究表明，在外源Fn存在的情况下，巨噬细胞对金黄色葡萄球菌的吞噬作用会增强。我们最近发现，FnBPs的过表达也会增强吞噬活性。本研究调查了金黄色葡萄球菌感染对巨噬细胞Fn表达的影响。
通过蛋白质印迹法测定了单核细胞（THP-1）、巨噬细胞、人肺腺癌（A549）细胞和肝癌（HepG2）细胞在金黄色葡萄球菌感染后分泌的Fn水平，结果显示仅在巨噬细胞中Fn分泌水平显著受到抑制。还通过蛋白质印迹法研究了巨噬细胞和HepG2细胞中与Fn调节相关的信号通路的激活情况。在巨噬细胞和HepG2细胞中Erk均被激活，而Src-JNK-c-Jun信号通路仅在巨噬细胞中被激活。在外源Fn存在的情况下，观察到金黄色葡萄球菌感染会导致巨噬细胞活力显著下降。
金黄色葡萄球菌感染会激活巨噬细胞中的Src-JNK-c-Jun信号通路，导致Fn表达受到抑制。这种抑制可能在巨噬细胞抵抗金黄色葡萄球菌感染中发挥保护作用。本研究首次证明金黄色葡萄球菌感染会抑制巨噬细胞中的Fn表达。
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