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首页> 外文期刊>The European Journal of Neuroscience >LPS/IFN-gamma cytotoxicity in oligodendroglial cells: role of nitric oxide and protection by the anti-inflammatory cytokine IL-10.
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LPS/IFN-gamma cytotoxicity in oligodendroglial cells: role of nitric oxide and protection by the anti-inflammatory cytokine IL-10.

机译：少突胶质细胞中的LPS /IFN-γ细胞毒性：一氧化氮的作用和抗炎细胞因子IL-10的保护作用。

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Proinflammatory mediators have been implicated in demyelinating disorders, including multiple sclerosis, whereas it has been proposed that the anti-inflammatory cytokines interleukin- (IL-) 4 and IL-10 participate in disease recovery. The present study analysed the effect of interferon-gamma (IFN-gamma) and bacterial endotoxin (lipopolysaccharide, LPS) on proliferation and survival of progenitors and differentiated oligodendrocytes. We also investigated the presence of receptors for IL-4 and IL-10 in oligodendroglial cells and explored a possible protective action of IL-4 and IL-10 in cultures following LPS/IFN-gamma. Finally, the role of endogenous nitric oxide (NO) on cell viability and the modulatory action of IL-4 and IL-10 on inducible nitric oxide synthase (iNOS) expression were also analysed. We report that LPS and/or IFN-gamma reduced proliferation and viability of oligodendroglial cells. Cell death, presumably by apoptosis as evidence by TUNEL and Annexin V binding, was observed following LPS/IFN-gamma, progenitors being more sensitive than differentiated cells. At both developmental stages, LPS/IFN-gamma-treated cultures expressed iNOS protein and released micromolar concentrations of NO. In progenitors, LPS/IFN-gamma-mediated cell damage was partially dependent on endogenous NO production, whereas NO was fundamental for cytotoxicity of differentiated oligodendrocytes. Both cell types expressed mRNA for IL-4 and IL-10 receptors and expression of IL-10 receptors at the protein level was also demonstrated. Treatment with either cytokine inhibited the expression of iNOS resulting from the proinflammatory stimulation. IL-10 was more effective than IL-4 in suppressing iNOS expression and, interestingly, IL-10 conferred protection against oligodendroglial death evoked by LPS/IFN-gamma. Our data raise the question of whether IL-10 may play a protective role in demyelinating diseases, not only downregulating the function of inflammatory cells but also promoting survival of progenitors and differentiated oligodendrocytes.
机译：促炎性介质与包括多发性硬化症在内的脱髓鞘疾病有关，而已提出抗炎细胞因子白介素（IL-）4和IL-10参与疾病的恢复。本研究分析了干扰素-γ（IFN-γ）和细菌内毒素（脂多糖，LPS）对祖细胞和分化少突胶质细胞的增殖和存活的影响。我们还研究了少突胶质细胞中IL-4和IL-10受体的存在，并探讨了LPS /IFN-γ后培养物中IL-4和IL-10的可能的保护作用。最后，还分析了内源性一氧化氮（NO）对细胞活力的作用以及IL-4和IL-10对诱导型一氧化氮合酶（iNOS）表达的调节作用。我们报告LPS和/或IFN-γ减少少突胶质细胞的增殖和活力。 LPS /IFN-γ后，观察到细胞死亡，大概是通过凋亡作为TUNEL和膜联蛋白V结合的证据，祖细胞比分化的细胞更敏感。在两个发育阶段，LPS /IFN-γ处理的培养物均表达iNOS蛋白并释放出微摩尔浓度的NO。在祖细胞中，LPS /IFN-γ介导的细胞损伤部分取决于内源性NO的产生，而NO对于分化的少突胶质细胞的细胞毒性至关重要。两种细胞类型都表达了IL-4和IL-10受体的mRNA，并且还证明了IL-10受体在蛋白质水平上的表达。用任一种细胞因子处理均抑制了由促炎性刺激引起的iNOS的表达。 IL-10在抑制iNOS表达方面比IL-4更有效，有趣的是，IL-10可以保护LPS /IFN-γ引起的少突胶质细胞死亡。我们的数据提出了一个问题，即IL-10是否可能在脱髓鞘疾病中起保护作用，不仅下调炎症细胞的功能，而且还促进祖细胞和分化的少突胶质细胞的存活。

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