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标题：Changes in Neutrophil Fatty Acid Composition and Its Relationship to Function Following Burn Injury in Humans
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作者：Vera C. PRATT ; Edward E. TREDGET ; M. Thomas CLANDININ 等
期刊名称：Journal of Clinical Biochemistry and Nutrition
印刷版ISSN：0912-0009
电子版ISSN：1880-5086
出版年度：2002
卷号：31
页码：45-58
DOI：10.3164/jcbn.31.45
出版社：The Society for Free Radical Research Japan
摘要：Membrane lipid composition influences a number of immune functions including those of neutrophils, an important defense against infection after burn injury that has also been implicated in causing damage to host tissues. This study investigates compositional changes in phospholipid (PL) fatty acids and functional alterations of neutrophils immediately following and during recovery from burn injury. Ten patients with>10% total body surface area burn had blood drawn at specific times (0 days to>50 days) following burn injury. Neutrophil lipids were extracted, major PL classes separated by thin layer chromatography, and fatty acid composition determined using gas liquid chromatography. Neutrophil granularity and oxidative burst were measured in whole blood before and after stimulation with phorbol myristate acetate using flow cytometry. Neutrophils were less granular and had a greater oxidative burst early (<20 days) vs. later (>50 days) after burn injury. The arachidonic acid (20: 4n-6) content in all PL fractions was significantly reduced following burn injury and increased with recovery ( p <0.05). The total n-6 fatty acid content of PS and PI increased with recovery ( p <0.05). In conclusion, reduced 20: 4n-6 in neutrophil PL is suggestive of increased release or reduced synthesis of 20: 4n-6 early after burn. Lower granularity and higher oxidative burst immediately post-injury normalized with increases in 20: 4n-6. Compositional changes in neutrophil membranes early after burn may impact effector functions of neutrophils. Further work is needed to develop nutritional intervention strategies designed to modulate fatty acid composition of neutrophils to reduce the harmful effects of the oxidative burst while maintaining important infection defense mechanisms following burn injury.