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Immunomodulatory intervention with Gamma interferon in mice with sepsis

机译：用败血症用γ干扰素用γ干扰素的免疫调节干预

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Abstract Aims Sepsis-triggered immune paralysis including T-cell dysfunction increase susceptibility to infection. Gamma interferon (IFNg) exert beneficial effects in patients with sepsis. Herein, we speculated that IFNg may attenuate T-cell dysfunction induced by sepsis, although the mechanisms remain elusive. To test this hypothesis, we used a model based on cecal ligation and puncture (CLP) to induce sepsis in mice. Main methods Male C57BL/6 mice were pretreated with recombinant human IFNg (0.01 μg/g of body weight) before CLP. The immunophenotyping of cell surface receptor expression, and regulatory T cells (CD4 + CD25 + Foxp3 +) were quantified by flow cytometry. Immunohistochemical staining was performed to evaluate the loss of immune effector cells. Formation of IFNg and interleukin 4 (IL-4) in the spleen and plasma levels of TNF-α, IL-6, high-mobility group box 1 (HMGB1) were determined using enzyme-linked immunosorbent assay. Key findings IFNg markedly inhibited the reduction in cytokine secretion from lipopolysaccharide (LPS)-stimulated splenocytes. IFNg-treated mices had significantly decreased percentages of programmed cell death 1 (PD-1) receptors, increased the percentages of positive costimulatory receptor CD28 on CD4 T cells expressing. IFNg markedly reduced T-cell apoptosis through upregulating the expression of Bcl-2. CLP-induced formation of regulatory T cells in the spleen was abolished in IFNg -treated mices. Moreover, IFNg treatment reduced plasma levels of TNF-α, IL-6, HMGB1. Significance IFNg can be a powerful regulator of immune function under sepsis conditions. Therefore, targeted immune-enhancement with IFNg may be a valid therapeutic approach in sepsis. ]]>
机译：摘要旨在脓毒症触发免疫瘫痪，包括T细胞功能障碍增加了对感染的敏感性。 γ干扰素（IFNG）对败血症患者发挥有益效果。在此，我们推测IFNG可以衰减败血症诱导的T细胞功能障碍，尽管机制仍然难以捉摸。为了测试这一假设，我们使用基于盲肠结扎和穿刺（CLP）的模型来诱导小鼠的败血症。主要方法在CLP之前用重组人IFNG（0.01μg/ g体重）预处理雄性C57BL / 6小鼠。通过流式细胞术定量细胞表面受体表达和调节性T细胞（CD4 + CD25 + FOXP3 +）的免疫蛋白型。进行免疫组织化学染色以评估免疫效应细胞的损失。使用酶联免疫吸附测定法测定IFG和白细胞介素4（IL-4）的TNF-α，IL-6，高迁移率组箱1（HMGB1）的血浆水平。主要发现IFNG显着抑制了脂多糖（LPS）刺激的脾细胞的细胞因子分泌的减少。 IFG治疗的MICE具有显着降低的编程细胞死亡1（PD-1）受体的百分比，增加了表达CD4 T细胞的正性刺激受体CD28的百分比。 IFNG通过上调Bcl-2的表达明显降低T细胞凋亡。 CLP诱导脾脏中调节性T细胞的形成被废除在IFNG -Treated Mices中。此外，IFG治疗降低了TNF-α，IL-6，HMGB1的血浆水平。 IFNG在败血症条件下，IFNG可以是免疫功能的强大调节因子。因此，具有IFNG的靶向免疫增强可能是败血症中有效的治疗方法。 ]]>

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