Ediger D, Sin B A, Heper A, Anadolu Y, Misirligil Z
Department of Allergic Diseases, School of Medicine, Ankara University, Ankara 06530, Turkey.
Clin Exp Allergy. 2005 Mar;35(3):319-26. doi: 10.1111/j.1365-2222.2005.02194.x.
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.
鼻息肉病（NP）是上呼吸道的一种慢性炎症性疾病，常与哮喘并存。然而，尤其是NP患者的发病机制仍存在争议。
为了更好地理解这种关系中涉及的免疫病理机制，我们研究了单纯NP患者以及合并哮喘的NP患者支气管和鼻组织中的炎症细胞谱。
选择17例NP患者（男性6例，女性11例，年龄范围：19 - 63岁，平均年龄：38.29±13.27岁）进行研究。根据是否存在哮喘或支气管高反应性（BHR）将受试者分为两组。无BHR的NP患者（第1组）（n = 8），NP合并哮喘或BHR的患者（第2组）（n = 9）。所有患者均接受特应性评估，包括详细病史、皮肤点刺试验（SPT）、血清总IgE和特异性IgE测定。在研究前至少1个月，所有受试者均未使用吸入、鼻用或口服糖皮质激素。哮喘患者的呼吸道症状仅在需要时使用短效β₂ - 激动剂吸入药物控制。使用纤维内镜从所有患者中获取NP组织、鼻和支气管黏膜活检标本。通过免疫组织化学方法测定标本中表达CD3、CD8、CD16、CD68、AA1（肥大细胞类胰蛋白酶）、人类白细胞抗原 - DR（HLA - DR）和嗜酸性粒细胞过氧化物酶（EPO）的细胞。对阳性染色的炎症细胞类型进行计数。分别评估上皮下固有层和腺周区域。
两组之间息肉组织、鼻和支气管中CD3⁺、CD8⁺、CD16⁺、CD68⁺、AA1⁺、HLA - DR⁺和EPO⁺阳性细胞数量无显著差异。在所有组中，息肉组织和鼻黏膜中CD8⁺、CD16⁺、HLA - DR⁺、EPO⁺细胞数量均显著高于支气管黏膜（P < 0.05）。然而，与合并哮喘和NP的患者相比，单纯NP患者的息肉组织和支气管黏膜中CD8⁺细胞显著增加（P < 0.
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