C Rudack1, F Sachse, J Alberty. 1. Department of Otorhinolaryngology, Head and Neck Surgery, University of Münster, Kardinal-von-Galen Ring 10, 48149 Muenster, Germany. rudack@uni-muenster.de
Abstract
OBJECTIVE AND DESIGN: The etiology and classification of chronic rhinosinusitis with and without nasal polyps still remain unclear. Based on investigations of inflammation type in biopsies from patients with nasal polyposis and chronic non-polypous rhinosinusitis, we tried to determine whether there is a need for further classification of chronic rhinosinusitis into two disease entities. SUBJECTS: Biopsies of diffuse nasal polyposis (n= 37) and chronic rhinosinusitis without nasal polyps (n= 41) were examined for eosinophil and neutrophil tissue infiltration, degree of inflammation, and involved cytokines in inflammation mechanisms. METHODS: Neutrophil elastase positive neutrophils and CD38-positive lymphocytes were characterized in nasal polyposis and chronic non-polypous rhinosinusitis by immunohistochemistry. Using a monoclonal antibody against eosinophilic cationic protein (ECP) activated eosinophils were identified. In tissue homogenates, albumin was quantified as a marker for inflammation vascular permeability. In addition, interleukin (IL)-8 and IL-5 were determined by means of quantitative ELISA measurements in homogenates. RESULTS: Significantly increased numbers of eosinophils and neutrophils were detected in nasal polyposis. In chronic rhinosinusitis without nasal polyps, tissue infiltration was dominated by lymphocytes and neutrophils. The concentration of albumin and IL-5 was significantly higher in nasal polyps than in chronic rhinosinusitis without nasal polyps. IL-8 protein levels did not differ significantly between the two tissue types. In addition, patients' durations of illness did not differ significantly. CONCLUSIONS: Different types and quantities of inflammatory cells as well as different levels of inflammation support our hypothesis that there is need for further subdivision of chronic rhinosinusitis into two disease entities.
OBJECTIVE AND DESIGN: The etiology and classification of chronic rhinosinusitis with and without nasal polyps still remain unclear. Based on investigations of inflammation type in biopsies from patients with nasal polyposis and chronic non-polypous rhinosinusitis, we tried to determine whether there is a need for further classification of chronic rhinosinusitis into two disease entities. SUBJECTS: Biopsies of diffuse nasal polyposis (n= 37) and chronic rhinosinusitis without nasal polyps (n= 41) were examined for eosinophil and neutrophil tissue infiltration, degree of inflammation, and involved cytokines in inflammation mechanisms. METHODS: Neutrophil elastase positive neutrophils and CD38-positive lymphocytes were characterized in nasal polyposis and chronic non-polypous rhinosinusitis by immunohistochemistry. Using a monoclonal antibody against eosinophilic cationic protein (ECP) activated eosinophils were identified. In tissue homogenates, albumin was quantified as a marker for inflammation vascular permeability. In addition, interleukin (IL)-8 and IL-5 were determined by means of quantitative ELISA measurements in homogenates. RESULTS: Significantly increased numbers of eosinophils and neutrophils were detected in nasal polyposis. In chronic rhinosinusitis without nasal polyps, tissue infiltration was dominated by lymphocytes and neutrophils. The concentration of albumin and IL-5 was significantly higher in nasal polyps than in chronic rhinosinusitis without nasal polyps. IL-8 protein levels did not differ significantly between the two tissue types. In addition, patients' durations of illness did not differ significantly. CONCLUSIONS: Different types and quantities of inflammatory cells as well as different levels of inflammation support our hypothesis that there is need for further subdivision of chronic rhinosinusitis into two disease entities.
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