title: Pathogenesis of nasal polyps: an update.
abstract: The cause of nasal polyp formation is still unknown. Genetic predisposition has been suggested, but there are scanty data to support such theories. Activated epithelial cells may be the major source of mediators inducing influx of inflammatory cells (mostly eosinophils) and proliferation and activation of fibroblasts leading to nasal polyp formation. Infectious agents (including viruses, bacteria, or fungi) may be potential primary factors activating nasal epithelial cells. Proinflammatory cytokines and growth factors play important roles in the persistence of mucosal inflammation associated with nasal polyps. Arachidonic acid metabolites seem to be particularly important in the pathogenesis of nasal polyps in patients with aspirin hypersensitivity rhinosinusitis/asthma syndrome.
authors.affiliation: Department of Clinical Immunology and Allergy, Medical University of Lodz, 251 Pomorska Street, Building C5, Room 46, 92213 Lodz, Poland.
authors.forename: Rafal
authors.initials: R
authors.lastname: Pawliczak
authors.forename: Anna
authors.initials: A
authors.lastname: Lewandowska-Polak
authors.forename: Marek L
authors.initials: ML
authors.lastname: Kowalski
mesh_terms: D001241:Aspirin / Q000009:adverse effects; D018407:Bacterial Physiological Phenomena; D016207:Cytokines / Q000276:immunology; D004804:Eosinophils / Q000276:immunology; D005347:Fibroblasts / Q000378:metabolism; D005658:Fungi / Q000502:physiology; D020022:Genetic Predisposition to Disease; D006801:Humans; D006967:Hypersensitivity / Q000150:complications / Q000209:etiology; D007249:Inflammation / Q000276:immunology; D009297:Nasal Mucosa / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D009298:Nasal Polyps / Q000209:etiology*; D018406:Virus Physiological Phenomena
chemical_list: D016207:Cytokines; D001241:Aspirin