Eosinophils in the pathophysiology of nasal polyposis.
Nasal polyposis can be defined as a chronic inflammatory disease of the paranasal sinus mucosa, leading to a protrusion of benign edematous polyps from the meatus into the nasal cavities. Nasal polyps are histologically characterized by massive edema and accumulation of eosinophils. IgE-mediated allergy seems to play only a minor role in eosinophil accumulation, leaving the place for a new concept of non-allergic rhinitis with eosinophilia. The central question still remains, however, why eosinophils accumulate into nasal polyposis tissue. Some initial data show that tissue structural cells, i.e. epithelial cells or fibroblasts, could produce cytokines (GM-CSF) and play a role in eosinophil accumulation (micro-environmental theory). However, further studies showed, that GM-CSF was mainly produced by eosinophils themselves (autocrine theory), leading to the hypothesis of an intrinsic eosinophilic inflammatory process. Eosinophils may contribute to nasal polyp formation and growth not only through inflammation but also by exerting their effects on extracellular matrix including stimulation of collagen synthesis. Another feature associated with nasal polyposis is aspirin sensitivity. Some preliminary data indicate that eosinophils could also be involved in aspirin-sensitivity mechanisms.
Jankowski
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Department of ENT-Head and Neck Surgery, Central Hospital, Henri Poincaré University, Nancy, France.
D015703:Antigens, CD / Q000276:immunology; D001241:Aspirin / Q000009:adverse effects; D004804:Eosinophils / Q000276:immunology*; D005347:Fibroblasts; D016178:Granulocyte-Macrophage Colony-Stimulating Factor / Q000276:immunology; D006801:Humans; D006967:Hypersensitivity / Q000209:etiology; D009298:Nasal Polyps / Q000209:etiology*; D012333:RNA, Messenger; D012220:Rhinitis / Q000276:immunology
D015703:Antigens, CD; D012333:RNA, Messenger; D016178:Granulocyte-Macrophage Colony-Stimulating Factor; D001241:Aspirin