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首页> 外文期刊>Pulmonary Circulation >Sickle Erythrocytes and Platelets Augment Lung Leukotriene Synthesis with Downregulation of Anti-Inflammatory Proteins: Relevance in the Pathology of the Acute Chest Syndrome:
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Sickle Erythrocytes and Platelets Augment Lung Leukotriene Synthesis with Downregulation of Anti-Inflammatory Proteins: Relevance in the Pathology of the Acute Chest Syndrome:

机译：镰状红细胞和血小板增强肺白三烯合成与抗炎蛋白的下调：急性胸腔综合征的病理相关性：

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Initiation, progression, and resolution of vaso-occlusive pain episodes in sickle cell disease (SCD) have been recognized as reperfusion injury, which provokes an inflammatory response in the pulmonary circulation. Some 5-lipoxygenase (5-lox) metabolites are potent vasoconstrictors in the pulmonary circulation. We studied stimulation of production of the inflammatory eicosanoids leukotrienes (LTs) and prostaglandin E2 (PGE2) by isolated rat lungs perfused with sickle (HbSS) erythrocytes. Our hypothesis is that HbSS erythrocytes produce more LTs than normal (HbAA) erythrocytes, which can induce vaso-occlusive episodes in SCD patients. Lung perfusates were collected at specific time points and purified by high-pressure liquid chromatography, and LTC4 and PGE2 contents were measured by enzyme-linked immunosorbent assay (ELISA). Rat lung explants were also cultured with purified HbAA and HbSS peptides, and 5-lox, cyclooxygenase 1/2, and platelet-activating factor receptor (PAFR) proteins were measured by Western blotting, while prostacyclin and LTs produced by cultured lung explants were measured by ELISA. Lung weight gain and blood gas data were not different among the groups. HbSS-perfused lungs produced more LTC4 and PGE2 than HbAA-perfused lungs: 10.40 ± 0.62 versus 0.92 ± 0.2 ng/g dry lung weight (mean ± SEM; P = 0.0001) for LTC4. Inclusion of autologous platelets (platelet-rich plasma) elevated LTC4 production to 12.6 ± 0.96 and 7 ± 0.60 ng/g dry lung weight in HbSS and HbAA perfusates, respectively. HbSS lungs also expressed more 5-lox and PAFR. The data suggest that HbSS erythrocytes and activated platelets in patient's pulmonary microcirculation will enhance the synthesis and release of the proinflammatory mediators LTC4 and PGE2, both of which may contribute to onset of the acute chest syndrome in SCD.
机译：镰状细胞病（SCD）中血管闭塞性疼痛发作的发生，进展和缓解已被认为是再灌注损伤，它在肺循环中引起炎症反应。一些5-脂氧合酶（5-lox）代谢产物是肺循环中有效的血管收缩剂。我们研究了镰状（HbSS）红细胞灌流的分离大鼠肺对炎症性类花生酸白三烯（LTs）和前列腺素E2（PGE2）的刺激作用。我们的假设是HbSS红细胞比正常（HbAA）红细胞产生更多的LT，这可以在SCD患者中诱发血管闭塞性发作。在特定时间点收集肺灌注液，并通过高压液相色谱法纯化，并通过酶联免疫吸附测定（ELISA）测定LTC4和PGE2的含量。还用纯化的HbAA和HbSS肽培养大鼠肺外植体，并通过Western印迹法测量5-lox，环氧合酶1/2和血小板活化因子受体（PAFR）蛋白，同时测量由培养的肺外植体产生的前列环素和LTs。通过ELISA。两组之间的肺增重和血气数据没有差异。灌注HbSS的肺比灌注HbAA的肺产生更多的LTC4和PGE2：LTC4的肺干重为10.40±0.62对0.92±0.2 ng / g（平均±SEM; P = 0.0001）。在HbSS和HbAA灌流液中，包括自体血小板（富含血小板的血浆）将LTC4产量分别提高至干肺重12.6±0.96和7±0.60 ng / g。 HbSS肺也表达更多的5-lox和PAFR。数据表明，患者肺微循环中的HbSS红细胞和活化的血小板将增强促炎性介质LTC4和PGE2的合成和释放，两者均可能导致SCD急性胸腔综合征的发作。

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