首页> 外文期刊>American Journal of Physiology >Role of macrophage migration inhibitory factor in bleomycin-induced lung injury and fibrosis in mice.
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Role of macrophage migration inhibitory factor in bleomycin-induced lung injury and fibrosis in mice.

机译:巨噬细胞迁移抑制因子在博来霉素诱导的小鼠肺损伤和纤维化中的作用。

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摘要

Macrophage migration inhibitory factor (MIF) is a unique cytokine that reportedly overrides the anti-inflammatory effect of endogenous glucocorticoids. MIF has been demonstrated to be involved in a variety of inflammatory diseases. In this study, we examined the role of MIF in bleomycin (BLM)-induced lung injury and fibrosis. The levels of MIF in lung tissues and bronchoalveolar lavage fluids were significantly increased in the period 5-10 days after intratracheal administration of BLM. Treatment with the anti-MIF antibody significantly reduced the mortality at 14 days and the histopathological lung injury score at 10 days. These effects were accompanied with significant suppression of the accumulation of inflammatory cells in the alveolar space and tumor necrosis factor-alpha in the lungs at 7 days. However, the anti-MIF antibody did not affect either the content of lung hydroxyproline or the histopathological lung fibrosis score at 21 days after BLM. These data provide further evidence for the crucial role of MIF in acute lung inflammation but do not support the involvement of MIF in lung fibrosis induced by BLM in mice.
机译:巨噬细胞迁移抑制因子(MIF)是一种独特的细胞因子,据报道它能克服内源性糖皮质激素的抗炎作用。已经证明MIF与多种炎性疾病有关。在这项研究中,我们检查了MIF在博来霉素(BLM)诱导的肺损伤和纤维化中的作用。气管内施用BLM后5-10天,肺组织和支气管肺泡灌洗液中MIF的水平显着升高。用抗MIF抗体治疗可显着降低14天时的死亡率和10天时的组织病理学肺损伤评分。这些作用伴随着第7天肺泡空间炎性细胞积累和肺中肿瘤坏死因子-α的大量抑制。但是,抗MIF抗体不会影响BLM后21天时肺羟脯氨酸的含量或组织病理学肺纤维化评分。这些数据为MIF在急性肺部炎症中的关键作用提供了进一步的证据,但不支持MIF参与小鼠BLM诱导的肺纤维化。

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