Aspirin Intolerance: Experimental Models for Bed-to-Bench
Identifieur interne : 000885 ( Main/Exploration ); précédent : 000884; suivant : 000886Aspirin Intolerance: Experimental Models for Bed-to-Bench
Auteurs : Masamichi YamashitaSource :
- Current Drug Targets [ 1389-4501 ] ; 2016.
Abstract
Aspirin is the oldest non-steroidal anti-inflammatory drug (NSAID), and it sometimes causes asthma-like symptoms known as aspirin-exacerbated respiratory disease (AERD), which can be serious. Unwanted effects of aspirin (aspirin intolerance) are also observed in patients with food-dependent exercise-induced anaphylaxis, a type I allergy disease, and aspirin-induced urticaria (AIU). However the target and the mechanism of the aspirin intolerance are still unknown. There is no animal or cellular model of AERD, because its pathophysiological mechanism is still unknown, but it is thought that inhibition of cyclooxygenase by causative agents leads to an increase of free arachidonic acid, which is metabolized into cysteinyl leukotrienes (cysLTs) that provoke airway smooth muscle constriction and asthma symptoms. As the bed-to-bench approach, to confirm the clinical discussion in experimental cellular models, we have tried to develop a cellular model of AERD using activated RBL-2H3 cells, a rat mast cell like cell line. Indomethacin (another NSAID and also causes AERD), enhances in vitro cysLTs production by RBL-2H3 cells, while there is no induction of cysLTs production in the absence of inflammatory activation. Since this suggests that all inflammatory cells with activation of prostaglandin and cysLT metabolism should respond to NSAIDs, and then I have concluded that aspirin intolerance should be separated from subsequent bronchoconstriction. Evidence about the cellular mechanisms of NSAIDs may be employed for development of in vitro AERD models as the approach from bench-to-bed.
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DOI: 10.2174/1389450117666161005152327
PubMed: 27719658
PubMed Central: 5345322
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Aspirin Intolerance: Experimental Models for Bed-to-Bench</title><author><name sortKey="Yamashita, Masamichi" sort="Yamashita, Masamichi" uniqKey="Yamashita M" first="Masamichi" last="Yamashita">Masamichi Yamashita</name></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">27719658</idno><idno type="pmc">5345322</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5345322</idno><idno type="RBID">PMC:5345322</idno><idno type="doi">10.2174/1389450117666161005152327</idno><date when="2016">2016</date><idno type="wicri:Area/Pmc/Corpus">000761</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000761</idno><idno type="wicri:Area/Pmc/Curation">000761</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">000761</idno><idno type="wicri:Area/Pmc/Checkpoint">000295</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Checkpoint">000295</idno><idno type="wicri:Area/Ncbi/Merge">000576</idno><idno type="wicri:Area/Ncbi/Curation">000576</idno><idno type="wicri:Area/Ncbi/Checkpoint">000576</idno><idno type="wicri:doubleKey">1389-4501:2016:Yamashita M:aspirin:intolerance:experimental</idno><idno type="wicri:Area/Main/Merge">000887</idno><idno type="wicri:Area/Main/Curation">000885</idno><idno type="wicri:Area/Main/Exploration">000885</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Aspirin Intolerance: Experimental Models for Bed-to-Bench</title><author><name sortKey="Yamashita, Masamichi" sort="Yamashita, Masamichi" uniqKey="Yamashita M" first="Masamichi" last="Yamashita">Masamichi Yamashita</name></author></analytic><series><title level="j">Current Drug Targets</title><idno type="ISSN">1389-4501</idno><idno type="eISSN">1873-5592</idno><imprint><date when="2016">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Aspirin is the oldest non-steroidal anti-inflammatory drug (NSAID), and it sometimes causes asthma-like symptoms known as aspirin-exacerbated respiratory disease (AERD), which can be serious. Unwanted effects of aspirin (aspirin intolerance) are also observed in patients with food-dependent exercise-induced anaphylaxis, a type I allergy disease, and aspirin-induced urticaria (AIU). However the target and the mechanism of the aspirin intolerance are still unknown. There is no animal or cellular model of AERD, because its pathophysiological mechanism is still unknown, but it is thought that inhibition of cyclooxygenase by causative agents leads to an increase of free arachidonic acid, which is metabolized into cysteinyl leukotrienes (cysLTs) that provoke airway smooth muscle constriction and asthma symptoms. As the bed-to-bench approach, to confirm the clinical discussion in experimental cellular models, we have tried to develop a cellular model of AERD using activated RBL-2H3 cells, a rat mast cell like cell line. Indomethacin (another NSAID and also causes AERD), enhances in vitro cysLTs production by RBL-2H3 cells, while there is no induction of cysLTs production in the absence of inflammatory activation. Since this suggests that all inflammatory cells with activation of prostaglandin and cysLT metabolism should respond to NSAIDs, and then I have concluded that aspirin intolerance should be separated from subsequent bronchoconstriction. Evidence about the cellular mechanisms of NSAIDs may be employed for development of in vitro AERD models as the approach from bench-to-bed.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Samter, M" uniqKey="Samter M">M. Samter</name></author><author><name sortKey="Beers, R F" uniqKey="Beers R">R.F. Beers</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Widal, F" uniqKey="Widal F">F. Widal</name></author><author><name sortKey="Abrami, P" uniqKey="Abrami P">P. 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