Nicholas V.C. Ralston , Patricia C. Schmid , Harald H.O. Schmid
{"title":"激动剂刺激的肺泡巨噬细胞甘油磷脂酰基转换","authors":"Nicholas V.C. Ralston , Patricia C. Schmid , Harald H.O. Schmid","doi":"10.1016/S0005-2760(98)00065-4","DOIUrl":null,"url":null,"abstract":"<div><p>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 <sup>18</sup>O from H<sub>2</sub><sup>18</sup>O-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.</p></div>","PeriodicalId":100162,"journal":{"name":"Biochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"1998-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0005-2760(98)00065-4","citationCount":"2","resultStr":"{\"title\":\"Agonist-stimulated glycerophospholipid acyl turnover in alveolar macrophages\",\"authors\":\"Nicholas V.C. Ralston , Patricia C. Schmid , Harald H.O. Schmid\",\"doi\":\"10.1016/S0005-2760(98)00065-4\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><p>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 <sup>18</sup>O from H<sub>2</sub><sup>18</sup>O-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.</p></div>\",\"PeriodicalId\":100162,\"journal\":{\"name\":\"Biochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1998-07-31\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1016/S0005-2760(98)00065-4\",\"citationCount\":\"2\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Biochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S0005276098000654\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Biochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0005276098000654","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
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.