一項(xiàng)研究發(fā)現(xiàn),，人們對(duì)阿司匹林的反應(yīng)各異可能為炎癥和痊愈的個(gè)體差異提供了線索,。
Derek Gilroy及其同事使用除疣貼讓人類志愿者的前臂出現(xiàn)了水泡，然后評(píng)估了受試者的痊愈過程,。這組作者發(fā)現(xiàn),，此前對(duì)低劑量的阿司匹林顯示抗炎癥應(yīng)答的人表現(xiàn)出了在72小時(shí)內(nèi)水皰的生長和痊愈，而那些免疫系統(tǒng)對(duì)阿司匹林沒有反應(yīng)的人出現(xiàn)了痊愈更慢的水皰,。已知阿司匹林能夠促進(jìn)稱為脂氧素 ( lipoxins) 的炎癥控制分子的制造,。
該研究發(fā)現(xiàn)，水皰痊愈更快的人比水皰在72小時(shí)內(nèi)沒有痊愈的人的脂氧素基準(zhǔn)濃度更低。這組作者提出,，發(fā)出開始痊愈的指示可能在天然產(chǎn)生高量脂氧素的人的體內(nèi)飽和,，而脂氧素濃度低的人們的免疫系統(tǒng)可能受到阿司匹林或外傷引發(fā)的炎癥的刺激，從而表現(xiàn)出更迅速的炎癥消退和痊愈,。
這組作者說,，這項(xiàng)研究可能幫助科學(xué)家根據(jù)個(gè)體免疫應(yīng)答從而為患者定制抗炎癥治療。（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.
