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2014 ; 193
(1
): 41-7
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Aspirin activation of eosinophils and mast cells: implications in the
pathogenesis of aspirin-exacerbated respiratory disease
#MMPMID24890720
Steinke JW
; Negri J
; Liu L
; Payne SC
; Borish L
J Immunol
2014[Jul]; 193
(1
): 41-7
PMID24890720
show ga
Reactions to aspirin and nonsteroidal 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 nonsteroidal anti-inflammatory drugs. Activation was evaluated as
Ca2+ 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 Ca2+ flux
and PGD2 release. LysASA induced Ca2+ 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 Ca2+ flux and PGD2 release. AERD is associated
with eosinophils maturing locally in a high IFN-? milieu. As such, in additional
studies, eosinophil progenitors were differentiated in the presence of IFN-?
prior to activation with aspirin. Eosinophils matured in the presence of IFN-?
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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