| Literature DB >> 23639708 |
Tanya M Laidlaw1, Joshua A Boyce.
Abstract
Physiologic and pharmacologic studies support the hypothesis that aspirin-exacerbated respiratory disease (AERD) involves fundamental dysregulation in the production of and end-organ responsiveness to both antiinflammatory eicosanoids (prostaglandin E2) and proinflammatory effectors (cysteinyl leukotrienes). The acquired nature of AERD implies a disturbance in a potential epigenetic control mechanism of the relevant mediator systems, which may be a result of incompletely clarified environmental factors (eg, viral or bacterial infections, inhaled pollutants).Entities:
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Year: 2012 PMID: 23639708 PMCID: PMC3781366 DOI: 10.1016/j.iac.2012.11.006
Source DB: PubMed Journal: Immunol Allergy Clin North Am ISSN: 0889-8561 Impact factor: 3.479