首页> 外文期刊>American Journal of Physiology >Perfluorocarbon attenuates response of concanavalin A-stimulated mononuclear blood cells without altering ligand-receptor interaction.
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Perfluorocarbon attenuates response of concanavalin A-stimulated mononuclear blood cells without altering ligand-receptor interaction.

机译:全氟化碳可减弱伴刀豆球蛋白A刺激的单核血细胞的反应,而不会改变配体-受体的相互作用。

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Intrapulmonary application of perfluorocarbons (PFC) in acute lung injury is associated with anti-inflammatory effects. A direct impact on leukocytic function may be involved. To further elucidate PFC effects on cellular activation, we compared in an in vitro model the response of concanavalin A (ConA)-stimulated lymphocytes and monocytes exposed to perfluorohexane. We hypothesized that perfluorohexane attenuates the action of the lectin ConA by altering stimulant-receptor interaction on the cell surface. Mononuclear blood cells were stimulated by incubation with ConA in the presence of different amounts of perfluorohexane. The response of lymphocytes and monocytes was determined by means of IL-2 secretion and tissue factor (TF) expression, respectively. The influence of perfluorohexane on cell-surface binding of fluorescence-labeled ConA was studied using flow cytofluorometry and fluorescence microscopy. Perfluorohexane itself did not induce a cellular activation but significantly inhibited both monocytic TF expression and, to a far greater extent, IL-2 secretion of ConA-stimulated mononuclear blood cells. The effect of perfluorohexane was due neither to an alteration of cell viability nor to a binding of the stimulant. The amount of cell surface-bound ConA was not altered by perfluorohexane, and the overall pattern of ConA receptor rearrangement did not differ between controls and treated cells. In the present study, we provide further evidence for an anti-inflammatory effect of PFC that might be beneficial in states of pulmonary hyperinflammation. A PFC-induced alteration of stimulant-receptor interaction on the surface membrane does not seem to be the cause of attenuated cell activation.
机译:肺内全氟化碳(PFC)在急性肺损伤中的应用与抗炎作用有关。可能涉及对白细胞功能的直接影响。为了进一步阐明PFC对细胞活化的影响,我们在体外模型中比较了伴刀豆球蛋白A(ConA)刺激的淋巴细胞和暴露于全氟己烷的单核细胞的反应。我们假设全氟己烷通过改变细胞表面上的兴奋剂-受体相互作用来减弱凝集素ConA的作用。通过在不同量的全氟己烷存在下与ConA孵育来刺激单核血细胞。分别通过IL-2分泌和组织因子(TF)表达确定淋巴细胞和单核细胞的应答。使用流式细胞仪和荧光显微镜研究了全氟己烷对荧光标记的ConA细胞表面结合的影响。全氟己烷本身不会诱导细胞活化,但会显着抑制单核细胞TF的表达,并在很大程度上抑制ConA刺激的单核血细胞的IL-2分泌。全氟己烷的作用既不是由于细胞活力的改变也不是由于刺激剂的结合。全氟己烷不会改变细胞表面结合的ConA的量,而且对照和处理过的细胞之间ConA受体重排的总体模式也没有差异。在本研究中,我们为PFC的抗炎作用提供进一步的证据,它可能在肺部过度炎症的状态中有益。 PFC诱导的表面膜上刺激剂-受体相互作用的改变似乎不是细胞活化减弱的原因。

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