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Release of granulocyte-macrophage colony stimulating factor by human cultured airway smooth muscle cells: suppression by dexamethasone

机译:人培养的气道平滑肌细胞释放粒细胞-巨噬细胞集落刺激因子:地塞米松抑制

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摘要

Smooth muscle cells represent a significant percentage of the total cells in the airway but their contribution to the inflammatory response seen in airway disease has not been studied. Hence, we have looked at the release of the cytokine granulocyte-macrophage colony stimulating factor (GM-CSF) in response to bacterial lipopolysaccharide (LPS) and the pro-inflammatory cytokines interleukin-1β (IL-1β), tumour necrosis factor α (TNFα) and interferon γ (IFNγ). Human airway smooth muscle (HASM) cells released GM-CSF under basal conditions (45.4±13.1 pg ml−1) that was significantly enhanced by IL-1β and TNFα with a maximal effect seen at 10 ng ml−1 (1.31±0.07 ng ml−1 and 0.72±0.16 ng ml−1, respectively). In contrast, neither LPS nor IFNγ produced a significant increase in GM-CSF release. However, HASM cells exposed to IL-1β, TNFα and IFNγ generated more GM-CSF than that evoked by any cytokine alone (2.2±0.15 ng ml−1). The release of GM-CSF elicited by the cytokine mixture was inhibited by cycloheximide and dexamethasone. These data suggest that HASM cells might play an active part in initiating and/or perpetuating airway inflammation in addition to controlling airway calibre.
机译:平滑肌细胞占气道总细胞的很大百分比,但尚未研究它们对气道疾病中炎症反应的贡献。因此,我们研究了响应细菌脂多糖(LPS)和促炎细胞因子白介素-1β(IL-1β),肿瘤坏死因子α( TNFα)和干扰素γ(IFNγ)。人的气道平滑肌(HASM)细胞在基础条件下(45.4±13.1μgml -1 )释放GM-CSF,IL-1β和TNFα显着增强了这种状态,在10μngml时发挥最大作用 -1 (分别为1.31±0.07ngngml -1 和0.72±0.16ngngml -1 )。相反,LPS和IFNγ均未使GM-CSF释放显着增加。但是,暴露于IL-1β,TNFα和IFNγ的HASM细胞产生的GM-CSF比任何单独的细胞因子引起的多(2.2±0.15 ngmlml -1 )。细胞因子混合物引起的GM-CSF的释放被环己酰亚胺和地塞米松抑制。这些数据表明,除了控制气道口径以外,HASM细胞还可能在引发和/或持久性气道炎症中发挥作用。

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