Nasal polyposis: an update

Abstract

Nasal polyposis is a chronic inflammatory disease of the upper airway characterized histologically by the infiltration of inflammatory cells like eosinophils or neutrophils. Several hypotheses have been put forward regarding the underlying mechanisms including chronic infection, aspirin intolerance, alteration in aerodynamics with trapping of pollutants, epithelial disruptions, epithelial cell defects/gene deletions (CFTR gene), inhalant or food allergies. The present review is an update on the pathomechanisms of nasal polyposis. In the majority of nasal polyps, eosinophils comprise more than 60% of the cell population. Besides eosinophils, mast cells and activated T cells are also increased. An increased production of cytokines/chemokines like granulocyte/macrophage colony-stimulating factor, IL-5, RANTES and eotaxin contribute to eosinophil migration and survival. Increased levels of IL-8 can induce neutrophil infiltration. Increased expression of vascular endothelial growth factor and its upregulation by transforming growth factor-beta can contribute to the edema and increased angiogenesis in nasal polyps. Again, transforming growth factor-beta can modulate fibroblast function and thus contribute to eosinophil infiltration and stromal fibrosis. Other mediators like albumin, histamine and immunoglobulins IgE and IgG are also increased in nasal polyps. In addition, the local production of IgE in nasal polyps can contribute to the increased recurrence of nasal polyps via the IgE-mast cell-FcepsilonRI cascade. Finally, mast cell/T cell-epithelial cell/fibroblast interactions can contribute to the persistent eosinophilic inflammation seen in polyps. Thus although nasal polyposis is a multifactorial disease with several different etiological factors, chronic persistent inflammation is undoubtedly a major factor irrespective of the etiology.