Expression of transforming growth factors-α and β 1 messenger RNA and product by eosinophils in nasal polyps
Nasal polyps are thought to develop as a manifestation of a chronic inflammatory process involving the upper airways. The eosinophil characteristically represents a prominent component of the inflammatory cell infiltrate of these lesions. However, the major clinical problem associated with nasal pol...
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Veröffentlicht in: | Journal of allergy and clinical immunology 1994-05, Vol.93 (5), p.864-869 |
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Zusammenfassung: | Nasal polyps are thought to develop as a manifestation of a chronic inflammatory process involving the upper airways. The eosinophil characteristically represents a prominent component of the inflammatory cell infiltrate of these lesions. However, the major clinical problem associated with nasal polyps, nasal obstruction, reflects the proliferation of the stromal and epithelial elements, which constitute the bulk of these lesions. We recently reported that blood eosinophils of patients with hypereosinophilia can produce the cytokines transforming growth factors-α (TGF-α) and β
1 (TGF-β
1). These cytokines have many biologic activities, which include the regulation of epithelial proliferation, the promotion of extracellular matrix formation, and the induction of angiogenesis. We therefore used in situ hybridization to determine whether the eosinophils that infiltrate nasal polyps express TGF-α and/or TGF-β
1 messenger RNA and used immunohistochemistry to determine whether these eosinophils also express TGF-α and TGF-β
1, proteins. We found that eosinophils represented a major source of both transforming growth factors in each case of nasal polyposis examined and that in most cases the majority of all eosinophils expressed both TGF-α and TGF-β
1. These results suggest that production of TGF-α and TGF-β
1 by the infiltrating eosinophils may contribute to some of the pathologic changes observed in nasal polyposis, such as thickening of the epithelial basement membrane, stromal fibrosis, angiogenesis, and epithelial and glandular hyperplasia. |
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ISSN: | 0091-6749 1097-6825 |
DOI: | 10.1016/0091-6749(94)90379-4 |