Intranasal steroids decrease eosinophils but not mucin expression in nasal polyps

被引:34
作者
Burgel, PR
Cardell, LO
Ueki, IF
Nadel, JA
机构
[1] Univ Calif San Francisco, Cardiovasc Res Inst, San Francisco, CA 94143 USA
[2] Univ Paris 05, Hop Cochin, Serv Pneumol, Paris, France
[3] Malmo Univ Hosp, Dept Otorhinolaryngol, Malmo, Sweden
[4] Univ Calif San Francisco, Dept Physiol & Med, San Francisco, CA 94143 USA
关键词
airway epithelium; epidermal growth factor receptor; interleukin-8; leukocyte recruitment; mucous hypersecretion; steroid treatment;
D O I
10.1183/09031936.04.00014404
中图分类号
R56 [呼吸系及胸部疾病];
学科分类号
摘要
Increased mucin expression is a feature of nasal polyposis. Corticosteroids reduce polyp size and symptoms, but their effect on mucin production remains unknown. In this study, the effects of intranasal corticosteroids on MUC5AC mucin expression, nasal resistance, eosinophil and neutrophil infiltration, epidermal growth factor receptor (EGFR), interleukin (IL)-8, and tumour necrosis factor (TNF)-alpha expression was assessed in nasal polyps. In nine subjects, one nasal polyp was removed surgically before treatment and another was removed after 8 weeks of intranasal fluticasone (400 mug.day(-1)). Tissues were processed for in situ hybridisation and immunohistochemical staining. Described effects of fluticasone on nasal polyps (reduction in nasal resistance and in eosinophil infiltration) were evaluated. Morphometric analysis was performed to assess the effect of fluticasone on epithelial-, MUC5AC-, EGFR- and IL-8-stained areas, TNF-alpha-stained cells, and neutrophil numbers. Treatment with fluticasone decreased nasal resistance and intra-epithelial eosinophils. The MUC5AC-stained area in the epithelium was unchanged by treatment; MUC5AC mRNA expression was unaffected by treatment. EGFR-stained area, intraepithelial neutrophil numbers, IL-8 and TNF-alpha expression were also unchanged by therapy. Intranasal fluticasone was effective in decreasing nasal airflow resistance and intra-epithelial eosinophils but had no effect on mucin or epidermal growth factor receptor expression or on neutrophil recruitment.
引用
收藏
页码:594 / 600
页数:7
相关论文
共 31 条
[1]   Interleukin-8 expression in human nasal polyps [J].
Allen, JS ;
Eisma, R ;
Leonard, G ;
Lafreniere, D ;
Kreutzer, D .
OTOLARYNGOLOGY-HEAD AND NECK SURGERY, 1997, 117 (05) :535-541
[2]  
Burgel P.R., 2002, ASTHMA COPD BASIC ME, P155, DOI [10.1016/B978-012079028-9/50091-0, DOI 10.1016/B978-012079028-9/50091-0]
[3]   Relation of epidermal growth factor receptor expression to goblet cell hyperplasia in nasal polyps [J].
Burgel, PR ;
Escudier, E ;
Coste, A ;
Dao-Pick, T ;
Ueki, IF ;
Takeyama, K ;
Shim, JJ ;
Murr, AH ;
Nadel, JA .
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 2000, 106 (04) :705-712
[4]   Human eosinophils induce mucin production in airway epithelial cells via epidermal growth factor receptor activation [J].
Burgel, PR ;
Lazarus, SC ;
Tam, DCW ;
Ueki, IF ;
Atabai, K ;
Birch, M ;
Nadel, JA .
JOURNAL OF IMMUNOLOGY, 2001, 167 (10) :5948-5954
[5]  
Cohn L, 1999, J IMMUNOL, V162, P6178
[6]   Identification of MUC5B, MUC5AC and small amounts of MUC2 mucins in cystic fibrosis airway secretions [J].
Davies, JR ;
Svitacheva, N ;
Lannefors, L ;
Kornfält, R ;
Carlstedt, I .
BIOCHEMICAL JOURNAL, 1999, 344 :321-330
[7]   ICAM-1 expression in upper respiratory mucosa is differentially related to eosinophil and neutrophil inflammation according to the allergic status [J].
Demoly, P ;
Sahla, M ;
Campbell, AM ;
Bousquet, J ;
Crampette, L .
CLINICAL AND EXPERIMENTAL ALLERGY, 1998, 28 (06) :731-738
[8]   Effect of low-dose beclomethasone dipropionate on asthma control and airway inflammation [J].
Fahy, JV ;
Boushey, HA .
EUROPEAN RESPIRATORY JOURNAL, 1998, 11 (06) :1240-1247
[9]   Distribution of respiratory mucin proteins in human nasal mucosa [J].
Groneberg, DA ;
Peiser, C ;
Dinh, QT ;
Matthias, J ;
Eynott, PR ;
Heppt, W ;
Carlstedt, I ;
Witt, C ;
Fischer, A ;
Chung, KF .
LARYNGOSCOPE, 2003, 113 (03) :520-524
[10]   Expression of respiratory mucins in fatal status asthmaticus and mild asthma [J].
Groneberg, DA ;
Eynott, PR ;
Lim, S ;
Oates, T ;
Wu, R ;
Carlstedt, I ;
Roberts, P ;
McCann, B ;
Nicholson, AG ;
Harrison, BD ;
Chung, KF .
HISTOPATHOLOGY, 2002, 40 (04) :367-373