Human β-defensins and toll-like receptors in the upper airway

被引:115
作者
Claeys, S
de Belder, T
Holtappels, G
Gevaert, P
Verhasselt, B
van Cauwenberge, P
Bachert, C
机构
[1] Univ Ghent, Dept Otorhinolaryngol, B-9000 Ghent, Belgium
[2] Univ Ghent, Dept Clin Chem Microbiol & Immunol, B-9000 Ghent, Belgium
关键词
adenoids; chronic sinusitis; beta-defensins; innate immunity; lymphoid tissue; nasal polyps; polymerase chain reaction; toll-like receptor; tonsils;
D O I
10.1034/j.1398-9995.2003.00180.x
中图分类号
R392 [医学免疫学];
学科分类号
100102 ;
摘要
Background: Measurement of innate markers in nasal mucosa, tonsils and adenoids might lead to new views about the role of innate immunity in the upper airway. In this study, the expression of human beta-defensins (HBD) 2 and 3 and toll-like receptors (TLR) 2 and 4 in various upper airway diseases was investigated. Methods: Surgical samples from patients with tonsillar disease (n = 18), hypertrophic adenoids (n = 10) and sinonasal disease (n = 30) (chronic sinusitis, nasal polyps, turbinate mucosa as controls) were investigated by immunohistochemistry. Quantification of HBD-2 and 3 mRNA, TLR-2 and 4 mRNA expression was performed by real-time polymerase chain reaction (PCR). Results: Immunohistochemistry revealed a strong expression of HBD-2 in tonsillar tissue. Quantification of HBD-2 and HBD-3 mRNA showed a more than tenfold higher expression in tonsillar tissue than in adenoids, whereas in nasal biopsies, only negligible defensin expression could be measured. No significant differences were found for TLR-4 between the various tissues, whereas TLR-2 expression in adenoids was significantly lower compared with other tissues. Conclusion: These results demonstrate a strong defensin expression in tonsillar tissue compared with nasal and paranasal mucosa and adenoids. Toll-like receptor expression in all these tissues illustrates a possibly important immunological sentinel function of upper airway mucosa.
引用
收藏
页码:748 / 753
页数:6
相关论文
共 43 条
[1]   Toll-like receptors: critical proteins linking innate and acquired immunity [J].
Akira, S ;
Takeda, K ;
Kaisho, T .
NATURE IMMUNOLOGY, 2001, 2 (08) :675-680
[2]  
Ali RS, 2001, J INVEST DERMATOL, V117, P106
[3]   Bacterial fimbriae and their peptides activate human gingival epithelial cells through toll-like receptor 2 [J].
Asai, Y ;
Ohyama, Y ;
Gen, K ;
Ogawa, T .
INFECTION AND IMMUNITY, 2001, 69 (12) :7387-7395
[4]   Plasma and BAL fluid concentrations of antimicrobial peptides in patients with Mycobacterium avium-intracellulare infection [J].
Ashitani, J ;
Mukae, H ;
Hiratsuka, T ;
Nakazato, M ;
Kumamoto, K ;
Matsukura, S .
CHEST, 2001, 119 (04) :1131-1137
[5]   CD14-dependent lipopolysaccharide-induced ß-defensin-2 expression in human tracheobronchial epithelium [J].
Becker, MN ;
Diamond, G ;
Verghese, MW ;
Randell, SH .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (38) :29731-29736
[6]   Synergy between TLR2 and TLR4: A safety mechanism [J].
Beutler, E ;
Gelbart, T ;
West, C .
BLOOD CELLS MOLECULES AND DISEASES, 2001, 27 (04) :728-730
[7]   SURFACE VS CORE-TONSILLAR AEROBIC AND ANAEROBIC FLORA IN RECURRENT TONSILLITIS [J].
BROOK, I ;
YOCUM, P ;
SHAH, K .
JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 1980, 244 (15) :1696-1698
[8]   Differential alteration in intestinal epithelial cell expression of Toll-like receptor 3 (TLR3) and TLR4 in inflammatory bowel disease [J].
Cario, E ;
Podolsky, DK .
INFECTION AND IMMUNITY, 2000, 68 (12) :7010-7017
[9]   Lipopolysaccharide activates distinct signaling pathways in intestinal epithelial cell lines expressing toll-like receptors [J].
Cario, E ;
Rosenberg, IM ;
Brandwein, SL ;
Beck, PL ;
Reinecker, HC ;
Podolsky, DK .
JOURNAL OF IMMUNOLOGY, 2000, 164 (02) :966-972
[10]  
Claeys S, 1996, ACTA OTO-LARYNGOL, P40