While normal functioning neutrophils contribute in various, critical ways to the maintenance of a stable immune system, their hypo- or hyper-activation has been implicated in the onset or exacerbation of multiple inflammatory conditions often affecting the vulnerable, aging population. As such, many would benefit from interventions capable of targeting neutrophils in disease-specific ways without disrupting their primary role in maintaining immune function. After consumption, marine omega-3 fatty acids are rapidly incorporated into the phospholipid bilayer of neutrophils, changing the fatty acid composition and consequently modifying neutrophil function. In addition to eicosanoid synthesis, the mechanisms by which marine n-3 fatty acids and their metabolites alter neutrophil function involve blockage of transcription factors that subsequently reduce pro-inflammatory gene expression by neutrophils and through the disruption of lipid rafts. In the current mini-review, a brief explanation of marine n-3 fatty acid metabolism is provided and the subsequent impact on neutrophil function is discussed. In addition, current evidence of the effects of marine n-3 fatty acid supplementation on neutrophil function from clinical trials conducted in the past 15 years is summarized.

虽然正常功能的中性粒细胞以各种关键方式有助于维持稳定的免疫系统，但它们的低激活或高激活与经常影响脆弱的老龄化人口的多种炎症状况的发作或恶化有关。因此，许多人将从能够以疾病特异性方式靶向中性粒细胞而不破坏其在维持免疫功能中的主要作用的干预措施中受益。食用后，海洋 omega-3 脂肪酸会迅速结合到中性粒细胞的磷脂双层中，从而改变脂肪酸组成，从而改变中性粒细胞的功能。除了类花生酸合成，海洋 n-3 脂肪酸及其代谢物改变中性粒细胞功能的机制涉及转录因子的阻断，从而降低中性粒细胞的促炎基因表达，并通过破坏脂筏。在当前的小型回顾中，提供了对海洋 n-3 脂肪酸代谢的简要说明，并讨论了随后对中性粒细胞功能的影响。此外，总结了过去 15 年进行的临床试验中海洋 n-3 脂肪酸补充剂对中性粒细胞功能影响的当前证据。