Aspirin activation of eosinophils and mast cells: implications in the pathogenesis of aspirin-exacerbated respiratory disease.
Aspirin activation of eosinophils and mast cells: implications in the pathogenesis of aspirin-exacerbated respiratory disease.
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DOI：
10.4049/jimmunol.1301753
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发表时间：
2014-07-01
期刊：
影响因子：
--
通讯作者：
Borish L
中科院分区：
文献类型：
--
作者：
Steinke JW;Negri J;Liu L;Payne SC;Borish L
Reactions to aspirin and non-steroidal anti-inflammatory drugs in patients with aspirin-exacerbated respiratory disease (AERD) are triggered when constraints upon activated eosinophils, normally supplied by PGE2, are removed secondary to cyclooxygenase-1 inhibition. However, the mechanism driving the concomitant cellular activation is unknown. We investigated the capacity of aspirin itself to provide this activation signal. Eosinophils were enriched from peripheral blood samples and activated with lysine ASA (LysASA). Parallel samples were stimulated with related non-steroidal anti-inflammatory drugs. Activation was evaluated as Ca+2 flux, secretion of cysteinyl leukotrienes (CysLT), and eosinophil derived neurotoxin (EDN) release. CD34+ progenitor-derived mast cells were also used to test the influence of aspirin on human mast cells with measurements of Ca+2 flux and PGD2 release. LysASA induced Ca+2 fluxes and EDN release, but not CysLT secretion from circulating eosinophils. There was no difference in the sensitivity or extent of activation between AERD and control subjects and sodium salicylate was without effect. Like eosinophils, aspirin was able to activate human mast cells directly through Ca+2 flux and PGD2 release. AERD is associated with eosinophils maturing locally in a high interferon (IFN)-γ milieu. As such, in additional studies, eosinophil progenitors were differentiated in the presence of IFN-γ prior to activation with aspirin. Eosinophils matured in the presence of IFN-γ displayed robust secretion of both EDN and CysLTs. These studies identify aspirin as the trigger of eosinophil and mast cell activation in AERD, acting in synergy with its ability to release cells from the anti-inflammatory constraints of PGE2.
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影响因子：
14.2
作者：
Pérez-Novo, CA;Watelet, JB;Bachert, C
通讯作者：
Bachert, C
DOI：
10.1164/ajrccm.157.4.9707089
发表时间：
1998-04-01
影响因子：
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影响因子：
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DOI：
10.1073/pnas.1313185110
发表时间：
2013-10-15
影响因子：
11.1
作者：
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通讯作者：
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影响因子：
14.2
作者：
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通讯作者：
Stevenson, DD