The effect of aspirin desensitization on novel biomarkers in aspirin-exacerbated respiratory diseases

Katial, Rohit; Strand, Matthew; Prasertsuntarasai, T.; Leung, Roxanne S.; Zheng, Wei-Hong; Alam, Rafeul

doi:10.1016/j.jaci.2010.06.036

Cited by 60 publications

(62 citation statements)

References 43 publications

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“…Other NSAIDs, namely indomethacin and flurbiprofen, had no effect in inhibiting the synthesis of IL-4, but the very weak inhibitor of COX-1, salicylic acid, was at least as effective as aspirin in inhibiting IL-4 expression. In the current study by Katial et al, 10 the same IL-4-suppressive effects of aspirin were measured in all 21 study patients with AERD and in none of the 3 control subjects, suggesting impressive specificity for patients afflicted with AERD. If the effects of aspirin on IL-4 levels in patients with AERD are unique to the AERD population, it is unclear why this same effect could be detected in vitro in the cells of healthy donors.…”

supporting

confidence: 66%

“…Renewed interest in LTE 4 , which is released in such striking quantities in patients with AERD, with its own special receptor (CysLT E R) mediating vascular dilatation, might also hold the answer to some of the remaining questions. Our understanding of the pathogenesis of AERD, reactions, and its treatment is progressing nicely and is clearly enhanced by the study of Katial et al 10 Many new avenues for further investigation are also opening up before us.…”

mentioning

confidence: 99%

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Does suppression of IL-4 synthesis by aspirin explain the therapeutic benefit of aspirin desensitization treatment?

White¹,

Stevenson²

2010

Journal of Allergy and Clinical Immunology

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supporting

confidence: 66%

mentioning

confidence: 99%

Does suppression of IL-4 synthesis by aspirin explain the therapeutic benefit of aspirin desensitization treatment?

White¹,

Stevenson²

2010

Journal of Allergy and Clinical Immunology

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“…Direct inhibition of the IL-4-activated STAT6 pathway upon repetitive aspirin ingestion has also been described [48]. Furthermore, sputum IL-4 levels decreased in AERD patients 6 months after desensitization [49]. Aksu et al [50 & ] recently showed that aspirin desensitization decreased CD4 þ IFN-g and IL-10 levels after 1 month of treatment, suggesting that expression of these modulators by CD4 þ T lymphocytes may be associated with desensitization.…”

Section: Aspirin Desensitizationmentioning

confidence: 93%

Upper airways in aspirin-exacerbated respiratory disease

Choi

Kim

Park

2015

Current Opinion in Allergy &Amp; Clinical Immunology

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“…This does not preclude their participation in long-term events that control the propensity to have an adverse reaction. For example, there are observations suggesting that desensitisation to aspirin may cause chronic changes in the IL-4 pathway [39,40] that may regulate responsiveness to NSAIDs.…”

Section: Discussionmentioning

confidence: 99%

“…Thus, the aspirin/NSAID-induced asthmatic reaction is associated with the release of histamine [28,29,30], tryptase [9,29,30,39], PGD 2 [9,10,11,12,30] and CysLTs [7,8,9,10,11,12,13]. There are also histological findings [32] supporting the participation of mast cells in the intolerance reaction.…”

Section: Discussionmentioning

confidence: 99%

Challenge of Isolated Sputum Cells Supports in vivo Origin of Intolerance Reaction to Aspirin/Non-Steroidal Anti-Inflammatory Drugs in Asthma

Higashi¹,

Kumlin²,

Higashi³

et al. 2012

Int Arch Allergy Immunol

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Background: There is no in vitro test to diagnose aspirin-intolerant asthma (AIA). The aim of this study was to test if challenge with aspirin of sputum cells from subjects with AIA triggers the release of cysteinyl leukotrienes (CysLTs), known to be mediators of bronchoconstriction in AIA. Methods: Sputum induction was performed at baseline and at another visit 2 h after a lysine-aspirin bronchoprovocation in 10 subjects with AIA and 9 subjects with aspirin-tolerant asthma (ATA). The isolated sputum cells were incubated for ex vivo challenge. Results: Release of CysLTs by sputum cells from patients with AIA was not induced by lysine-aspirin ex vivo, neither when cells were collected at baseline nor in sputum cells recovered after lysine-aspirin-induced bronchoconstriction, whereas release of CysLTs from sputum cells was triggered by an ionophore on both occasions. However, the CysLT levels elicited by the ionophore were higher in the AIA group both at baseline (AIA vs. ATA: 3.3 vs. 1.6 ng/million cells; p < 0.05) and after the lysine-aspirin bronchoprovocation (3.9 vs. 1.7 ng/million cells; p < 0.05). This difference in the amount of CysLTs released between the groups appeared to be related to the number of eosinophils. Conclusions: Intolerance to aspirin could not be triggered in sputum cells isolated from subjects with AIA. Together with the previous inability to demonstrate intolerance to non-steroidal anti-inflammatory drugs in isolated blood cells, these results support the requirement of tissue-resident cells in the adverse reaction. However, ex vivo stimulation of sputum cells may be developed into a new test of capacity for LT release in inflammatory cells recovered from airways.

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The effect of aspirin desensitization on novel biomarkers in aspirin-exacerbated respiratory diseases

Cited by 60 publications

References 43 publications

Does suppression of IL-4 synthesis by aspirin explain the therapeutic benefit of aspirin desensitization treatment?

Does suppression of IL-4 synthesis by aspirin explain the therapeutic benefit of aspirin desensitization treatment?

Upper airways in aspirin-exacerbated respiratory disease

Challenge of Isolated Sputum Cells Supports in vivo Origin of Intolerance Reaction to Aspirin/Non-Steroidal Anti-Inflammatory Drugs in Asthma

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