Background: The immune-inducing effect of the quorum sensing (QS) molecule autoinducer-2 (AI-2) on macrophages has not been previously comprehensively studied.Methods: We performed proteomic analysis on macrophages cocultured with purified Fusobacterium nucleatum (F. nucleatum) AI-2 and performed western blot analysis to verify the differential protein expression. We further used the Gene Expression Profiling Interactive Analysis and Tumor Immune Estimation Resource databases to analyze the expression of differentially expressed proteins in microbial-associated digestive tract tumors.Results: Based on proteomic analysis, we identified 46 upregulated proteins and 11 downregulated proteins. The upregulated proteins were mostly inflammatory factors such as tumor necrosis factor ligand superfamily member 9 (TNFSF9). These proteins have a range of biological functions associated with the regulation of inflammatory responses, apoptosis and tumorigenesis. TNFSF9 is highly expressed in pancreatic adenocarcinoma (PAAD) tissues and is associated with M1 polarization of macrophages.Conclusions: Our data indicated that F. nucleatum AI-2 induced inflammatory responses and activated multiple signaling pathways in macrophages. TNFSF9 is the most significantly differentially expressed protein induced by F. nucleatum AI-2 and is involved in regulating immune cell infiltration in PAAD. Thus, AI-2 may become a new focus for studying the relationship between bacteria and cancer.

中文翻译：

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通过TMT蛋白质组学分析鉴定了在Fusobacterium nucleatum Autoinducer-2处理的巨噬细胞中的免疫诱导。

背景：群体感应（QS）分子自诱导物2（AI-2）对巨噬细胞的免疫诱导作用尚未得到全面研究。方法：我们对与纯化的核梭形核杆菌（F. nucleatum）共培养的巨噬细胞进行了蛋白质组学分析。 AI-2并进行了蛋白质印迹分析以验证差异蛋白的表达。我们进一步使用基因表达谱交互式分析和肿瘤免疫估计资源数据库来分析差异表达的蛋白质在微生物相关的消化道肿瘤中的表达。结果：基于蛋白质组学分析，我们鉴定了46种上调的蛋白和11种下调的蛋白。上调的蛋白主要是炎性因子，例如肿瘤坏死因子配体超家族成员9（TNFSF9）。这些蛋白质具有与调节炎症反应，细胞凋亡和肿瘤发生有关的一系列生物学功能。TNFSF9在胰腺腺癌（PAAD）组织中高表达，并与巨噬细胞的M1极化相关。结论：我们的数据表明，核仁F. nucleatum AI-2诱导了巨噬细胞的炎症反应并激活了多种信号通路。TNFSF9是由F. nucleatum AI-2诱导的最显着差异表达的蛋白，参与调节PAAD中免疫细胞的浸润。因此，AI-2可能成为研究细菌与癌症之间关系的新焦点。TNFSF9在胰腺腺癌（PAAD）组织中高表达，并与巨噬细胞的M1极化有关。结论：我们的数据表明，核仁F. nucleatum AI-2诱导了巨噬细胞的炎症反应并激活了多种信号通路。TNFSF9是由F. nucleatum AI-2诱导的最显着差异表达的蛋白质，参与调节PAAD中免疫细胞的浸润。因此，AI-2可能成为研究细菌与癌症之间关系的新焦点。TNFSF9在胰腺腺癌（PAAD）组织中高表达，并与巨噬细胞的M1极化有关。结论：我们的数据表明，核仁F. nucleatum AI-2诱导了巨噬细胞的炎症反应并激活了多种信号通路。TNFSF9是由F. nucleatum AI-2诱导的最显着差异表达的蛋白质，参与调节PAAD中免疫细胞的浸润。因此，AI-2可能成为研究细菌与癌症之间关系的新焦点。