探讨沉默蛋白磷酸酶2cm（Pp2cm）基因对金黄色葡萄球菌（S. aureus）感染巨噬细胞炎症因子表达的影响及其机制。敲低Pp2cm对炎症因子、增殖、凋亡及Toll的影响在 RAW 264.7 细胞（一种用腺病毒 (Ad) 转染的鼠巨噬细胞系）中分析了样受体 (TLR) 信号传导。将细胞分为四组，包括Ad-Ctrl组、Ad-Pp2cm组、Ad-Ctrl金黄色葡萄球菌组和Ad-Pp2cm金黄色葡萄球菌组。通过单独引入对照腺病毒(Ad-Ctrl)或靶向Pp2cm基因的腺病毒(Ad-Pp2cm)来实现细胞转染，并且通过施加或不施加金黄色葡萄球菌来诱导炎症或不存在炎症。肿瘤坏死因子-α（TNF-α）、白细胞介素-1β（IL-1β）、TLR2、TLR4、Toll样受体衔接蛋白（Tirap）和骨髓分化因子88（Myd88）的表达通过real-时间荧光定量聚合酶链反应（RT-qPCR）。通过蛋白质印迹法测定PP2Cm蛋白表达。采用细胞计数试剂盒8（CCK-8）法检测细胞增殖情况，流式细胞仪检测细胞凋亡情况。与Ad-Ctrl组相比，Ad-Pp2cm组Pp2cm基因和PP2Cm蛋白表达下调，差异有统计学意义（P<0.05）。与Ad-Ctrl金黄色葡萄球菌组相比，Ad-Pp2cm金黄色葡萄球菌组巨噬细胞TNF-α和IL-1β基因水平显着升高（P<0.01）。此外，与Ad-Ctrl组相比，Ad-Pp2cm组巨噬细胞中TLR2、TLR4、Tirap和Myd88基因表达水平升高，差异有统计学意义（P<0.05）。 Ad-Ctrl组和Ad-Pp2cm组细胞凋亡和增殖差异无统计学意义。沉默Pp2cm基因促进巨噬细胞对金黄色葡萄球菌感染的炎症反应。此外，TLR通路在巨噬细胞炎症激活中发挥着重要作用。版权所有©四川大学学报（医学版）编委会。

To investigate the effect of silencing protein phosphatase 2cm ( Pp2cm) gene on the expression of inflammatory factors in macrophages infected with Staphylococcus aureus ( S. aureus) and the mechanisms involved.The effects of Pp2cm knockdown on inflammatory factors, proliferation, apoptosis, and Toll-like receptor (TLR) signaling were analyzed in RAW 264.7 cells, a murine macrophage cell line, transfected with adenovirus (Ad). The cells were divided into four groups, including Ad-Ctrl group, Ad- Pp2cm group, Ad-Ctrl+ S. aureus group and Ad- Pp2cm+ S. aureus group. Cell transfection was achieved by separately introducing control adenovirus (Ad-Ctrl) or adenovirus targeting the Pp2cm gene (Ad- Pp2cm) and inflammation or the absence of inflammation was induced by applying or not applying S. aureus. The expression of tumor necrosis factor-alpha ( TNF-α), interleukin-1β ( IL-1 β), TLR2, TLR4, Toll-like receptor adaptor protein ( Tirap) and myeloid differentiation factor 88 ( Myd88) was determined by real-time fluorescent quantitative polymerase chain reaction (RT-qPCR). PP2Cm protein expression was determined by Western blot. Cell proliferation was determined by cell counting kit-8 (CCK-8) assay and cell apoptosis was measured by flow cytometry.The expression of Pp2cmgene and PP2Cm protein was downregulated in the Ad- Pp2cm group when compared to the Ad-Ctrl group, with the diference showing statistical significance ( P<0.05). When compared to those of the Ad-Ctrl+ S. aureus group, macrophages in the Ad- Pp2cm+ S. aureus group showed significantly increase in the TNF- α and IL-1 β gene levels ( P<0.01). Furthermore, the Ad- Pp2cm group demonstrated elevated gene expression levels of TLR2, TLR4, Tirap and Myd88 in macrophages when compared to the Ad-Ctrl group, with the difference showing statistical significance ( P<0.05). There were no statistically significant differences in cell apoptosis and proliferation between the Ad-Ctrl and Ad- Pp2cm groups.Silencing Pp2cm gene promotes the inflammatory response of macrophages to S. aureus infection. Moreover, the TLR pathway plays an important role in the inflammatory activation of macrophages.Copyright© by Editorial Board of Journal of Sichuan University (Medical Sciences).