一項研究發現，人們對阿司匹林的反應各異可能為炎症和痊癒的個體差異提供了線索。
Derek Gilroy及其同事使用除疣貼讓人類志願者的前臂出現了水泡，然後評估了受試者的痊癒過程。這組作者發現，此前對低劑量的阿司匹林顯示抗炎症應答的人表現出了在72小時內水皰的生長和痊癒，而那些免疫系統對阿司匹林沒有反應的人出現了痊癒更慢的水皰。已知阿司匹林能夠促進稱為脂氧素 ( lipoxins) 的炎症控制分子的製造。
該研究發現，水皰痊癒更快的人比水皰在72小時內沒有痊癒的人的脂氧素基準濃度更低。這組作者提出，發出開始痊癒的指示可能在天然產生高量脂氧素的人的體內飽和，而脂氧素濃度低的人們的免疫系統可能受到阿司匹林或外傷引發的炎症的刺激，從而表現出更迅速的炎症消退和痊癒。
這組作者說，這項研究可能幫助科學家根據個體免疫應答從而為患者定製抗炎症治療。（生物谷Bioon.com）
生物谷推薦原文出處：
PNAS doi: 10.1073/pnas.1000373107
Dichotomy in duration and severity of acute inflammatory responses in humans arising from differentially expressed proresolution pathways
Thea Morrisa, Melanie Stablesa, Paul Colville-Nashb, Justine Newsona, Geoffrey Bellinganc, Patricia M. de Souzad, and Derek W. Gilroya,1
aCentre for Clinical Pharmacology and Therapeutics, Division of Medicine, University College London, London WC1E 6JJ, United Kingdom;
bSouth West Thames Institute for Renal Research, St. Helier Hospital, Carshalton SM5 1AA, United Kingdom;
cCritical Care, University College London Hospitals National Health Service Foundation Trust, London NW1 2BU, United Kingdom; and
dCardiothoracic Pharmacology Department, Airway Disease Section, National Heart and Lung Institute, Imperial College, London SW3 6LY, United Kingdom
Lipoxins (Lxs) and aspirin-triggered epi-Lxs (15-epi-LxA4) act through the ALX/FPRL1 receptor to block leukocyte trafficking, dampen cytokine/chemokine synthesis, and enhance phagocytic clearance of apoptotic leukocytes—key requisites for inflammatory resolution. Although studies using primarily inbred rodents have highlighted resolution as an active event, little is known about the role resolution pathways play in controlling the duration/profile of inflammatory responses in humans. To examine this, we found two types of responders to cantharidin-induced skin blisters in male healthy volunteers: those with immediate leukocyte accumulation and cytokine/chemokine synthesis followed by early resolution and a second group whose inflammation increased gradually over time followed by delayed resolution. In early resolvers, blister 15-epi-LxA4 and leukocyte ALX were low, but increased as inflammation abated. In contrast, in delayed resolvers, 15-epi-LxA4 and ALX were high early in the response but waned as inflammation progressed. Elevating 15-epi-LxA4 in early resolvers using aspirin increased blister leukocyte ALX but reduced cytokines/chemokines as well as polymorphonuclear leukocyte and macrophage numbers. These findings show that two phenotypes exist in humans with respect to inflammation severity/longevity controlled by proresolution mediators, namely 15-epi-LxA4. These data have implications for understanding the etiology of chronic inflammation and future directions in antiinflammatory therapy.