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Proteomic profiling of dextran sulfate sodium induced acute ulcerative colitis mice serum exosomes and their immunomodulatory impact on macrophages

机译：葡聚糖硫酸钠对急性溃疡性结肠炎小鼠血清外泌体的蛋白质组学分析及其对巨噬细胞的免疫调节作用

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Macrophages are essential for the maintenance of intestinal homeostasis, and their activation has been proposed to be critical to the pathogenesis of inflammatory bowel disease (IBD). Although there are many recognized mediators of macrophage activation, increasing evidence suggests that macrophages respond to exosome stimulation. Exosomes are 40-150 nm microvesicles released from different cell types and are found in a variety of physiological fluids, including serum. As studies have shown that circulating exosomes participate in intercellular communication and can mediate the immune response, we hypothesized that exosomes may play a role in the pathogenesis of IBD though modulation of macrophage activity. In this study, we used the dextran sulfate sodium (DSS) induced acute colitis mice model to investigate the effect of serum exosomes on macrophages and identify exosome proteins potentially involved in macrophage activation. We treated RAW264.7 macrophages with serum exosomes isolated from dextran sulfate sodium induced mice and found that treatment induced phosphorylation of p38 and ERK and production of tumor necrosis factor α when compared to treatment with exosomes isolated from control mice. Subsequent proteomic analysis identified 56 differentially expressed proteins, a majority of which were acute-phase proteins and immunoglobulins. Bioinformatics analysis suggested these proteins were mainly involved in the complement and coagulation cascade, which has been implicated in macrophage activation. Our findings provide new insight into the role of circulating serum exosomes in acute colitis and contribute to the understanding of macrophage activation in the pathogenesis of IBD.
机译：巨噬细胞对于维持肠内稳态是必不可少的，并且已经提出巨噬细胞的活化对于炎性肠病（IBD）的发病机理至关重要。尽管有许多公认的巨噬细胞激活介质，但越来越多的证据表明巨噬细胞对外来体刺激有反应。外泌体是从不同细胞类型释放的40-150 nm微囊泡，存在于多种生理液中，包括血清。研究表明，循环的外泌体参与细胞间通讯并可以介导免疫反应，我们假设外泌体可能通过调节巨噬细胞活性而在IBD的发病中发挥作用。在这项研究中，我们使用了右旋糖酐硫酸钠（DSS）诱导的急性结肠炎小鼠模型，以研究血清外泌体对巨噬细胞的影响，并确定可能参与巨噬细胞激活的外泌体蛋白。我们用从硫酸葡聚糖钠诱导的小鼠分离的血清外泌体处理RAW264.7巨噬细胞，发现与用对照小鼠分离的外泌体相比，该治疗诱导了p38和ERK的磷酸化以及肿瘤坏死因子α的产生。随后的蛋白质组分析确定了56种差异表达的蛋白质，其中大多数是急性期蛋白质和免疫球蛋白。生物信息学分析表明，这些蛋白主要参与补体和凝血级联反应，这与巨噬细胞活化有关。我们的发现为循环血清外来体在急性结肠炎中的作用提供了新的见识，并有助于了解巨噬细胞在IBD发病机理中的激活作用。

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