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Nasal mucosa inflammation pathways" denote the sum of molecular and cellular mechanisms mediating local immune responses and inflammation in the nasal epithelium. Central components include cytokine signaling (particularly the type 2 immune pathway involving IL-4, IL-5, IL-13), activation and recruitment of immune cells (eosinophils, mast cells, Th2 lymphocytes), and the resulting release of mediators such as histamine and leukotrienes. These pathways are fundamental to the pathogenesis of common nasal inflammatory diseases (allergic rhinitis, chronic rhinosinusitis with or without nasal polyps), and their dysregulation drives key symptoms like nasal congestion, mucus hypersecretion, and tissue remodeling. Numerous therapies target specific pathway components, such as intranasal corticosteroids, anti-cytokine monoclonal antibodies, and antihistamines, each aiming to suppress inflammatory responses and restore nasal mucosal homeostasis[3][4][5][6][7][1].
Glucocorticoids: suppression of prostaglandin and cytokine synthesis, inhibition of immune cell migration; Biologics: blockade of cytokine signaling (e.g., anti-IL-4 receptor, anti-IL-5, anti-IgE); Antihistamines: inhibition of histamine receptor signaling; Leukotriene modifiers: inhibition of leukotriene pathway and eosinophil activation
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