Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
9161914 | Chest | 2005 | 15 Pages |
Abstract
Systemically bioavailable leukotriene receptor antagonists (LTRAs) can reduce the essential components of allergic inflammation in allergic rhinitis (AR) and asthma by blocking cysteinyl leukotriene (CysLT) activity, resulting in a wide range of clinical effects. CysLTs, mediators, and modulators in the pathophysiology of asthma and AR are a key target for therapy because they modulate production of hemopoietic progenitor cells, survival and recruitment of eosinophils to inflamed tissue, activity of cytokines and chemokines, quantity of exhaled NO, smooth-muscle contraction, and proliferation of fibroblasts. The mechanism of action of LTRAs leads to their effects on systemic allergic inflammatory processes
Keywords
VCAMgranulocyte-macrophage colony–stimulating factorTNFPC20Type 2 T helperLTC4Cysteinyl leukotrieneCysLTLTD4Th2LTRAICAMGM-CSFICSPEFAUCAsthmaleukotriene receptor antagonistsLeukotriene receptor antagonistEosinophilsinflammationinterleukinRemodelingPeak expiratory flowRhinitisAllergic rhinitisCytokinesPlatelet-activating factortumor necrosis factorLeukotriene C4Leukotriene D4Leukotrienesintercellular adhesion moleculevascular cell adhesion moleculeNitric oxidePAFInhaled corticosteroid
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Authors
Busse MD, Kraft MD, FCCP,