Macrophage migration inhibitory factor exhibits a pronounced circadian rhythm relevant to its role as a glucocorticoid counter-regulator
Macrophage migration inhibitory factor exhibits a pronounced circadian rhythm relevant to its role as a glucocorticoid counter-regulator
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DOI：
10.1046/j.0818-9641.2002.01148.x
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发表时间：
2003-04-01
影响因子：
4
通讯作者：
Bucala, R
中科院分区：
文献类型：
--
作者：
Petrovsky, N;Socha, L;Bucala, R
在人类中，辅助性T细胞因子1的最大表达与血浆皮质醇的夜间最低点一致，而辅助性T细胞因子2的反应在白天占主导地位。促炎细胞因子巨噬细胞移动抑制因子对糖皮质激素介导的免疫抑制进行反调节。为了确定皮质醇和巨噬细胞移动抑制因子之间的关系，健康志愿者每小时抽血24小时，用于测量血浆皮质醇和基础和刺激的巨噬细胞移动抑制因子。与皮质醇相似，巨噬细胞移动抑制因子在上午晚些时候达到峰值，而干扰素-γ、肿瘤坏死因子-α、白细胞介素-1和白细胞介素-12则在夜间达到峰值。口服可的松后，血浆巨噬细胞移动抑制因子升高2-4倍，而其他细胞因子降低。胰岛素耐量试验中皮质醇与血浆巨噬细胞移动抑制因子无相关性。早晨晚些时候达到高峰的巨噬细胞移动抑制因子，通过拮抗皮质醇介导的促炎细胞因子抑制，可能延长清晨炎症的持续时间。这些观察结果解释了炎症性关节炎模型中巨噬细胞移动抑制因子中和的有益作用。
In humans, maximal expression of T helper 1 cytokines coincide with the nocturnal nadir of plasma cortisol, whereas T helper 2 cytokine responses are dominant during day-time. The pro-inflammatory cytokine, macrophage migration inhibitory factor counter-regulates glucocorticoid-mediated immune suppression. To determine the relationship between cortisol and macrophage migration inhibitory factor, healthy volunteers had blood drawn hourly for 24 h for measurement of plasma cortisol and basal- and stimulated-macrophage migration inhibitory factor. Similar to cortisol, macrophage migration inhibitory factor peaked during the late morning whereas interferon-gamma, tumour necrosis factor-alpha, interleukin-1 and interleukin-12 demonstrated a nocturnal peak. After oral cortisone, plasma macrophage migration inhibitory factor rose 2-4-fold, whereas the other cytokines decreased. There was no correlation between cortisol during the insulin tolerance test and plasma macrophage migration inhibitory factor. The late morning peak of macrophage migration inhibitory factor, by antagonizing cortisol-mediated pro-inflammatory cytokine suppression may prolong the duration of early morning inflammation. These observations explain the beneficial role of macrophage migration inhibitory factor neutralization in models of inflammatory arthritis.