9-cis Retinoic Acid Inhibits Inflammatory Responses of Adherent Monocytes and Increases Their Ability to Induce Classical Monocyte Migration
9-cis Retinoic Acid Inhibits Inflammatory Responses of Adherent Monocytes and Increases Their Ability to Induce Classical Monocyte Migration
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DOI：
10.1159/000332375
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发表时间：
2012-01-01
影响因子：
5.3
通讯作者：
Dahle, Maria K.
中科院分区：
文献类型：
--
作者：
Kolseth, Ingrid B. M.;Agren, Joanna;Dahle, Maria K.
患有维生素A/视黄醇缺乏症的患者被证明易于感染并患有炎症增加，这些影响可以通过维生素A补充剂来补救。我们的目的是研究如何从健康供体外周静脉血中的人单核细胞在粘附和暴露于细菌内毒素的存在或不存在的9-顺式异构体的视黄酸（9cisRA）后的最初几个小时内采取行动。我们发现粘附的人单核细胞主要是CD14 + CD16+亚型。用9cisRA预处理1小时显著降低了脂多糖（LPS）诱导的肿瘤坏死因子（TNF）α、白细胞介素（IL）-6和趋化因子配体（CCL）3和CCL 4的mRNA表达和蛋白释放。相反，用9cisRA处理快速增强单核细胞化学吸引蛋白/CCL2的产生。9cisRA处理还导致经典CD 14high单核细胞在transwell体外系统中的迁移增强。我们的结论是，9cisRA治疗人粘附单核细胞减弱炎症反应的LPS和诱导经典的单核细胞的吸引力，这可能有助于解释为什么补充剂给予维生素A缺乏的患者抵消炎症，并增加抗感染的能力。版权所有（C）2012 S. Karger AG，巴塞尔
Patients with vitamin A/retinol deficiency are shown to be prone to infections and to suffer from increased inflammation, effects which can be remedied by vitamin A supplements. We aimed to study how human monocytes from the peripheral venous blood of healthy donors acted within the initial hours after adherence and exposure to bacterial endotoxin in the presence or absence of the 9-cis-isomer of retinoic acid (9cisRA). We found that adherent human monocytes were dominated by the CD14dimCD16+ subtype. Pretreatment with 9cisRA for 1 h significantly decreased lipopolysaccharide (LPS)-induced mRNA expression and protein release of tumor necrosis factor (TNF)alpha, interleukin (IL)-6 and chemokine ligands (CCL)3 and CCL4. In contrast, treatment with 9cisRA rapidly enhanced the production of monocyte chemoattractive protein/CCL2. 9cisRA treatment also led to enhanced migration of classical CD14high monocytes in a transwell in vitro system. We conclude that 9cisRA treatment of human adherent monocytes attenuates the inflammatory responses to LPS and induces the attraction of classical monocytes, a feature which may help explain why supplements administered to vitamin A-deficient patients counteract inflammation and increases the ability to fight infections. Copyright (C) 2012 S. Karger AG, Basel