Nasal polyposis: Immunohistochemistry and bioelectrical findings (a hypothesis for the development of nasal polyps)

The pathophysiology of nasal polyp formation is unclear. Several theories have implicated chronic allergic rhinitis, genetic predisposition, autonomie dysfunction of the blood vessels of the nasal mucosa, and inflammation. Prior research from this group demonstrated that defects in sodium ion flux may cause water retention in nasal polyps. Based on this observation, the authors proposed that abnormal concentrations of inflammatory mediators present in nasal polyps might influence the function of both sodium and chloride channels at the luminal surfaces of nasal epithelial and nasal polyps. Subsequent modulation of ion flux by inflammatory mediators could lead to water retention and edema of the nasal mucosa and thus contribute to the production of polyposis. This particular study was conducted to answer the question whether the inflammatory cell population in polyps was different from that in inferior turbinâtes, and whether the cells that are recruited into nasal polyps might affect local pathophysiology. Nasal polyps and turbinâtes were obtained from individuals undergoing surgery for symptomatic nasal obstruction caused by nonatopic rhinosinusitis or allergic rhinosinusitis. A portion of the tissue from each patient was fixed and prepared for study for histochemical and immunohistochemical methods. Monoclonal antibodies were used to identify macrophages, lymphocytes, and plasma cells. Subsequently, the remainder of the tissue samples were treated with protease to disaggregate the epithelia, and the cells were then cultured. Transepithelial potential differences and resistance were measured daily. When the cells attained maximal transepithelial differences, they were mounted in Ussing chambers and exposed to sodium positive channel blockers and selected chloride negative channel agonists. Middle turbinâtes and polyps were found to have more macrophages, lymphocytes and plasma cells, HLA-DR positive cells, and eosinophils than the inferior turbinâtes. Epithelial cells obtained from polyps showed higher transepithelial potential differences and equivalent short circuit currents than turbinate cell cultures. The responses to sodium channel blockers and chloride channel agonists were also greater for polyp versus turbinate cultures. Based on the results of this study, the authors propose a new theory of pathogenesis of nasal polyps. They hypothesize that local release of inflammatory mediators could cause sodium absorption and chloride permeability to be higher in polyps than in turbinate epithelia. Increased sodium absorption is consistent with the hypothesis that epithelial fluid absorption contributes to the development of nasal polyps, and this occurs as a result of the increased recruitment of inflammatory cells that are present in nasal polyps tissue.