激动剂刺激的肺泡巨噬细胞甘油磷脂酰基转换

Nicholas V.C. Ralston , Patricia C. Schmid , Harald H.O. Schmid
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引用次数: 2

摘要

炎症化合物β-葡聚糖(一种颗粒激动剂)和单宁(一种可溶性激动剂)存在于棉尘中,当吸入时,会导致大量花生四烯酸从肺泡巨噬细胞释放出来。早期的研究表明,这些激动剂对花生四烯酸的释放和释放有不同的影响,只有单宁能抑制外源性花生四烯酸的摄取和结合,这表明对酰基化有抑制作用。在这里,我们使用了含h218o的培养基中18O的时间依赖性结合到甘油磷脂酰基中,作为静止和激动剂处理的兔肺泡巨噬细胞酰基转换的指标。磷脂酰肌醇(每小时约30%)和胆碱磷脂(每小时10-20%)的周转率最高。β-葡聚糖和单宁都能以2倍或更多的倍数刺激酰基转换,尤其是花生四烯酸的转换。我们得出结论,两种激动剂都不能通过抑制乙酰化来促进花生四烯酸在肺泡巨噬细胞中的积累和释放。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Agonist-stimulated glycerophospholipid acyl turnover in alveolar macrophages

The inflammatory compounds β-glucan, a particulate agonist, and tannin, a soluble agonist, are present in cotton dust and, when inhaled, cause massive arachidonic acid release from alveolar macrophages. Earlier work had shown that these agonists exhibit different effects on arachidonate liberation and release, and that only tannin inhibits the uptake and incorporation of exogenous arachidonic acid, suggesting inhibition of reacylation. Here we have used the time-dependent incorporation of 18O from H218O-containing media into glycerophospholipid acyl groups as an indicator of acyl turnover in resting and agonist-treated rabbit alveolar macrophages. Highest turnover rates were seen in phosphatidylinositol (∼30% per hour) and in choline phospholipids (10–20% per hour). Both β-glucan and tannin stimulated acyl turnover, especially arachidonic acid turnover, in these and other lipid classes by a factor of 2 or more. We conclude that neither agonist promotes arachidonic acid accumulation in and release from alveolar macrophages by inhibiting reacylation.

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