Proresolution lipid mediators in multiple sclerosis - differential, disease severity-dependent synthesis - a clinical pilot trial.
Proresolution lipid mediators in multiple sclerosis - differential, disease severity-dependent synthesis - a clinical pilot trial.
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DOI：
10.1371/journal.pone.0055859
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发表时间：
2013
期刊：
影响因子：
3.7
通讯作者：
Schwab JM
中科院分区：
文献类型：
--
作者：
Prüss H;Rosche B;Sullivan AB;Brommer B;Wengert O;Gronert K;Schwab JM
炎症的严重程度和寿命由内源性反调节信号控制。其中包括长链多不饱和脂肪酸（PUFA）衍生的脂质介质，其促进炎症的消退，这是恢复组织稳态的一个积极过程。确定高活动性和低活动性多发性硬化（MS）患者内源性脂质源性消退激动剂的产生是否受到不同的调节。在大学医院神经科进行配对研究。根据临床（复发频率）和临床旁（MRI病变，对比增强）标准，将10对年龄和性别匹配的复发缓解型MS患者分配到一组高度活跃或不太活跃的MS。使用LC-MS/MS脂质组学定量血清和脑脊液中的脂质介质。对关键花生四烯酸（ω-6）和二十二碳六烯酸（ω-6）衍生的介导物花生四烯酸（PG）、白三烯、羟基二十碳四烯酸（HETE）和消退激动剂脂氧素A4（LXA 4）、消退素D1（RvD 1）和神经保护素D1（NPD 1）的水平进行定量。在高度活跃的MS患者组中，15-HETE和PGE 2增加，这是15-脂氧合酶和环氧合酶途径的产物。促消退介质RvD 1显著上调，仅在高活性组中检测到NPD 1。LXA 4水平没有增加，在高度活跃的MS患者。脂质介质途径调节MS患者的脑脊液中的差异，这取决于疾病的严重程度。非详尽的或可能的“延迟”解决途径可能表明一个有缺陷的决议程序在高度活跃的MS患者。纵向分析需要异型这种差异分辨率的能力，这可能与疾病进展，寿命和最终终止。
The severity and longevity of inflammation is controlled by endogenous counter-regulatory signals. Among them are long-chain polyunsaturated fatty acid (PUFA)-derived lipid mediators, which promote the resolution of inflammation, an active process for returning to tissue homeostasis. To determine whether endogenous production of lipid-derived resolution agonists is regulated differentially in patients with highly active and less active multiple sclerosis (MS). Matched-pairs study in University hospital Neurology department. Based on clinical (relapse frequency) and paraclinical (MRI lesions, contrast enhancement) criteria, 10 pairs of age- and sex-matched patients with relapsing-remitting MS were assigned either to a group with highly active or less active MS. Lipid mediators were quantified in serum and cerebrospinal fluid using LC-MS/MS-based lipidomics. Levels of the key arachidonic (ω-6) and docosahexaenoic acid (ω-6)-derived mediators prostaglandins (PG), leukotrienes, hydroxyeicosatetraenoic acids (HETE) and resolution agonists lipoxin A4 (LXA4), resolvin D1 (RvD1) and neuroprotectin D1 (NPD1) were quantified. In the patient group with highly active MS, 15-HETE and PGE2 were increased, which are products of the 15-lipoxygenase and cyclooxygenase pathways. The proresolution mediator RvD1 was significantly upregulated and NPD1 was detected in the highly active group only. LXA4 levels were not increased in patients with highly active MS. Lipid mediator pathways are regulated differentially in the cerebrospinal fluid of MS patients, depending on disease severity. Non-exhaustive or possibly ‘delayed’ resolution pathways may suggest a defective resolution program in patients with highly active MS. Longitudinal analyses are required to hetero-typify this differential resolution capacity, which may be associated with disease progression, longevity and eventual termination.
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影响因子：
82.9
作者：
Yao, Chengcan;Sakata, Daiji;Narumiya, Shuh
通讯作者：
Narumiya, Shuh
DOI：
10.1073/pnas.0405445101
发表时间：
2004-10-19
影响因子：
11.1
作者：
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影响因子：
105.7
作者：
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影响因子：
32.4
作者：
Uderhardt, Stefan;Herrmann, Martin;Kroenke, Gerhard
通讯作者：
Kroenke, Gerhard
影响因子：
11.2
作者：
Polman CH;Reingold SC;Banwell B;Clanet M;Cohen JA;Filippi M;Fujihara K;Havrdova E;Hutchinson M;Kappos L;Lublin FD;Montalban X;O'Connor P;Sandberg-Wollheim M;Thompson AJ;Waubant E;Weinshenker B;Wolinsky JS
通讯作者：
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