Increased production of macrophage migration inhibitory factor by PBMCs of atopic dermatitis
Increased production of macrophage migration inhibitory factor by PBMCs of atopic dermatitis
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DOI：
10.1016/s0091-6749(99)70339-8
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发表时间：
1999-09-01
影响因子：
14.2
通讯作者：
Nishihira, J
中科院分区：
文献类型：
--
作者：
Shimizu, T;Abe, R;Nishihira, J
背景：特应性皮炎(AD)是一种慢性瘙痒性炎症性皮肤病。AD的潜在原因是多因素的，几种细胞因子被认为与这种严重的炎症性皮肤病有关。巨噬细胞移动抑制因子(MIF)是T细胞活化和迟发型超敏反应所必需的免疫调节细胞因子。最近我们发现AD患者血清MIF含量显著升高，与此相一致，湿疹皮损角质形成细胞MLF信使RNA表达上调。目的与方法：尽管角质形成细胞被认为是AD患者血清MIF含量升高的潜在来源，但在其他组织中还没有进行准确的评估。NIP广泛表达于多种细胞，包括T细胞和巨噬细胞。本研究通过检测AD患者外周血单个核细胞中MIF的产生及其信使RNA水平，探讨这些细胞在血清MIF含量升高中的作用及其与病理特征的关系。结果：与我们先前的研究结果一致，AD患者的血清MIF含量显著高于非特应性健康对照组和无湿疹的慢性荨麻疹患者。对于未经刺激的PBMCs，AD患者PBMC培养上清液中MIF含量(Mean+/-SEM)为40.4+/-8.4 ng/m L，显著高于健康对照组(6.6+/-1.1 ng/m l)和慢性荨麻疹患者(8.5+/-1.4 ng/m l)(P<；0.0001)。当刀豆蛋白A刺激外周血单核细胞时，AD患者PBMC产生MIF的能力明显高于对照组和慢性荨麻疹患者，其MIF产生与刀豆蛋白A刺激的比率与AD的严重程度显著相关。AD患者外周血中MIF mRNA的表达水平显著高于非特应性健康对照组。结论：目前的研究结果表明，PBMCs可能是AD患者血清MIF升高的重要来源。由于MIF具有诱导局部和全身炎症和免疫反应的潜能，因此可以想象，由PBMC产生的MIF可能会影响AD的局部和全身病理特征。
Background: Atopic dermatitis (AD) is a chronic pruritic inflammatory skin disorder. The underlying cause of AD is multifactorial, and several cytokines are considered to be involved in this severe inflammatory skin disease. Macrophage migration inhibitory factor (MIF) is an immunoregulatory cytokine essential for T-cell activation and delayed-type hypersensitivity. Recently we demonstrated that serum MIF content was significantly elevated in patients with AD, Consistent with this, expression of MLF messenger RNA in keratinocytes of the eczematous skin lesion was up-regulated.Objective and Method: Although keratinocytes are considered to be a potential source of increased serum MIF content in AD, precise evaluation has not been carried out in other tissues. NIP is ubiquitously expressed in various cells, including T cells and macrophages. In this study we examined MIF production and its messenger RNA level of PBMCs from patients with AD to investigate the contribution of these cells to elevated serum MIF content and to its pathologic characteristics.Results: Consistent with our previous findings, the serum MIF content of patients with AD was significantly elevated compared with nonatopic healthy control subjects and patients with chronic urticaria without eczema. As for the MIF productivity of unstimulated PBMCs, the MIF content in the culture medium of PBMCs obtained from patients with AD (40.4 +/- 8.4 ng/mL) (mean +/- SEM) was significantly increased compared with that from healthy control subjects (6.6 +/- 1.1 ng/mL) and patients with chronic urticaria (8.5 +/- 1.4 ng/ml) (P < .0001). When PBMCs were stimulated by concanavalin A, MIF production by PBMCs of patients with AD was more enhanced than in control subjects or patients with chronic urticaria, The increased ratio of MIF production by PBMCs in response to concanavalin A was significantly correlated with the severity of clinical features of AD. Supporting these results, the level of MIF mRNA in PMBCs of patients with AD was significantly higher than in nonatopic healthy control subjects.Conclusions: The current results showed that PBMCs should be an important source of increased serum MIF in AD. Because MIF has the potential to induce local and systemic inflammatory and immune responses, it is conceivable that MIF produced by PBMCs may affect Local and systemic pathologic features in AD.