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首页> 外文期刊>Clinical & developmental immunology. >Modulation of Th1/Th2 Immune Responses by Killed Propionibacterium acnes and Its Soluble Polysaccharide Fraction in a Type I Hypersensitivity Murine Model: Induction of Different Activation Status of Antigen-Presenting Cells
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Modulation of Th1/Th2 Immune Responses by Killed Propionibacterium acnes and Its Soluble Polysaccharide Fraction in a Type I Hypersensitivity Murine Model: Induction of Different Activation Status of Antigen-Presenting Cells

机译:在I型超敏性鼠模型中,被痤疮丙酸杆菌杀死的Th1 / Th2免疫应答及其可溶性多糖组分的调节:诱导抗原呈递细胞的不同激活状态

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摘要

Propionibacterium acnes (P. acnes) is a gram-positive anaerobic bacillus present in normal human skin microbiota, which exerts important immunomodulatory effects, when used as heat- or phenol-killed suspensions. We previously demonstrated that heat-killed P. acnes or its soluble polysaccharide (PS), extracted from the bacterium cell wall, suppressed or potentiated the Th2 response to ovalbumin (OVA) in an immediate hypersensitivity model, depending on the treatment protocol. Herein, we investigated the mechanisms responsible for these effects, using the same model and focusing on the activation status of antigen-presenting cells (APCs). We verified that higher numbers of APCs expressing costimulatory molecules and higher expression levels of these molecules are probably related to potentiation of the Th2 response to OVA induced by P. acnes or PS, while higher expression of toll-like receptors (TLRs) seems to be related to Th2 suppression. In vitro cytokines production in cocultures of dendritic cells and T lymphocytes indicated that P. acnes and PS seem to perform their effects by acting directly on APCs. Our data suggest that P. acnes and PS directly act on APCs, modulating the expression of costimulatory molecules and TLRs, and these differently activated APCs drive distinct T helper patterns to OVA in our model.
机译:痤疮丙酸杆菌(痤疮丙酸杆菌)是存在于正常人皮肤微生物群中的革兰氏阳性厌氧杆菌,当用作加热或苯酚杀死的悬浮液时发挥重要的免疫调节作用。我们先前证明,从细菌细胞壁中提取的热杀死的痤疮丙酸杆菌或其可溶性多糖(PS)在即时超敏模型中抑制或增强了Th2对卵白蛋白(OVA)的反应,具体取决于治疗方案。在本文中,我们使用相同的模型并着眼于抗原呈递细胞(APC)的激活状态,研究了造成这些效应的机制。我们证实,表达共刺激分子的较高数量的APC和这些分子的较高表达水平可能与痤疮丙酸杆菌或PS诱导的对OVA的Th2反应增强有关,而toll样受体(TLR)的较高表达似乎是与Th2抑制有关。树突状细胞和T淋巴细胞共培养物中的体外细胞因子产生表明痤疮丙酸杆菌和PS似乎通过直接作用于APC而发挥其作用。我们的数据表明痤疮丙酸杆菌和PS直接作用于APC,调节共刺激分子和TLR的表达,而这些不同激活的APC在我们的模型中向OVA驱动不同的T辅助模式。

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