Airway inflammation in nasal polyposis: immunopathological aspects of relation to asthma

Abstract

Nasal polyposis (NP) is a chronic inflammatory disorder of the upper respiratory tract, which is often coexist with asthma. However, the pathogenesis of especially in patients with NP is still a matter of debate. To better understand the immunopathologic mechanism involved in this relationship, we investigated the inflammatory cell profiles in bronchial and nasal tissues of patients with NP alone and with concomitant asthma. Seventeen patients with NP (six male, 11 female, age range: 19-63, mean age: 38.29+/-13.27 years) were selected for the study. Subjects were divided into two groups based on the presence of asthma or bronchial hyper-responsiveness (BHR). NP without BHR (Group 1) (n=8), NP and asthma or BHR (Group 2) (n=9). All patients underwent atopy evaluation including detailed history, skin prick test (SPT), total and specific IgE determination in sera. None of the subjects had taken inhaled, nasal or oral corticosteroids for at least 1 month before the study. Respiratory symptoms of asthmatic patients were controlled with only short acting beta(2)-agonist inhaler drugs as needed. NP tissue, nasal and bronchial mucosa biopsies were taken from all patients using fiberoptic endoscopy. CD3, CD8, CD16, CD68, AA1 (mast cell tryptase), human leucocyte antigen-DR (HLA-DR) and eosinophil peroxidase (EPO) expressing cells in specimens were determined by immunohistochemical methods. Positively staining inflammatory cell types were counted. Subepithelial lamina propria and periglandular areas were separately evaluated. No significant difference was found in polyp tissue, nasal and bronchial CD3(+), CD8(+), CD16(+), CD68(+), AA1(+), HLA-DR(+) and EPO(+) positive cells between groups. There were significantly higher numbers of CD8(+), CD16(+), HLA-DR(+), EPO(+) cells in the polyp tissue and nasal mucosa vs. the bronchial mucosa in all groups (P<0.05). However, CD8(+) cells were significantly increased in the polyp tissue and bronchial mucosa of patients with NP alone when compared with the patients with both asthma and NP (P<0.05). CD3(+), CD68(+) and CD16(+) cell counts were tended to be higher within the nasal polyp tissue of patients with isolated NP compared with counts within nasal and bronchial mucosa of patients with NP and asthma. Also, patients with isolated NP showed more HLA-DR(+) cells in the nasal polyp tissue and nasal mucosa than those of patients with NP and asthma. Immunoreactivity for EPO(+) eosinophils within the nasal and bronchial mucosa was more prominent in patients with NP and asthma compared with patients with NP alone. The number of EPO(+) eosinophils within the polyp tissue, nasal and bronchial mucosa was higher in the skin prick test negative (SPT -ve) group than the SPT positive (SPT +ve) ones. Our results demonstrate that infiltration of inflammatory cells in the nasal and the lower airways do not remarkably differ between patients with NP alone who has no evidence of BHR and asthmatic patients with NP. However, patients with SPT-ve NP reveal more intense eosinophilic inflammation in the entire respiratory mucosa.