Xu Weihua, Tian Keyin, Hu Shaowen, Chen Mingxiao, Zhang Meng
Department of Emergency, Anhui Provincial Children's Hospital , Hefei, Anhui, China.
Department of Neonatology, Anhui Provincial Children's Hospital , Hefei, Anhui, China.
Infect Immun. 2023 Oct 17;91(10):e0016623. doi: 10.1128/iai.00166-23. Epub 2023 Sep 28.
In this study, we examined the effect of deletion on macrophages in methicillin-resistant (MRSA) infection. MRSA-infected mice were employed for the experiments, and RAW264.7 cells were stimulated with MRSA for the experiments. Macrophage polarization was determined by flow cytometry and quantitative real-time PCR; macrophage phagocytosis was assessed by flow cytometry and laser scanning confocal microscopy; cell apoptosis was assessed by flow cytometry and western blotting. deletion markedly elevated macrophage phagocytosis and M2 macrophages in MRSA infection, which was accompanied by elevated expression of and and reduced expression of , tumor necrosis factor-α (, and deletion also inhibited macrophage apoptosis in MRSA infection, which was manifested by elevated B-cell lymphoma 2 (BCL-2) protein level and reduced protein levels of cleaved cysteine protease 3 (CASPASE-3) and BCL2-Associated X (BAX). Both the and experiments further showed the activation of phosphoinositide 3-kinase (PI3K)/AKT (also known as protein kinase B, PKB) signaling pathway in MRSA infection and that the regulation of expression may be dependent on Toll-like receptor (TLR) 2/PI3K pathway. The above results showed that deletion exhibited a protective role against MRSA infection by promoting M2 polarization and phagocytosis of macrophages and the regulation of partly owing to the activation of TLR2/PI3K pathway, proposing a novel therapeutic strategy for MRSA-infected pneumonia.
在本研究中，我们检测了[缺失基因名称]缺失对耐甲氧西林金黄色葡萄球菌（MRSA）感染中巨噬细胞的影响。实验采用MRSA感染的小鼠，并使用RAW264.7细胞用MRSA刺激进行实验。通过流式细胞术和定量实时PCR确定巨噬细胞极化；通过流式细胞术和激光扫描共聚焦显微镜评估巨噬细胞吞噬作用；通过流式细胞术和蛋白质印迹法评估细胞凋亡。[缺失基因名称]缺失显著提高了MRSA感染中巨噬细胞的吞噬作用和M2巨噬细胞比例，同时伴随着[相关基因名称1]和[相关基因名称2]表达升高以及[相关基因名称3]表达降低，肿瘤坏死因子-α（TNF-α）[相关情况]，并且[缺失基因名称]缺失还抑制了MRSA感染中巨噬细胞的凋亡，表现为B细胞淋巴瘤2（BCL-2）蛋白水平升高以及裂解的半胱氨酸蛋白酶3（CASPASE-3）和BCL2相关X蛋白（BAX）水平降低。[具体实验1]和[具体实验2]实验进一步表明在MRSA感染中磷酸肌醇3激酶（PI3K）/AKT（也称为蛋白激酶B，PKB）信号通路被激活，并且[相关基因名称]表达的调节可能依赖于Toll样受体（TLR）2/PI3K途径。上述结果表明，[缺失基因名称]缺失通过促进巨噬细胞的M2极化和吞噬作用以及[相关基因名称]的调节对MRSA感染发挥保护作用，部分原因是TLR2/PI3K途径的激活，为MRSA感染的肺炎提出了一种新的治疗策略。
