Up-regulation of Toll-like receptors 2, 3 and 4 in allergic rhinitis -: art. no. 100

被引:75
作者
Fransson, M [1 ]
Adner, M
Erjefält, J
Jansson, L
Uddman, R
Cardell, LO
机构
[1] Lund Univ, Malmo Univ Hosp, Dept Otorhinolaryngol, Lab Clin & Expt Allergy Res, Malmo, Sweden
[2] Lund Univ, Univ Lund Hosp, Dept Expt Med Sci, S-22100 Lund, Sweden
[3] AstraZeneca R&D, Lund, Sweden
关键词
D O I
10.1186/1465-9921-6-100
中图分类号
R56 [呼吸系及胸部疾病];
学科分类号
摘要
Background: Toll-like receptors enable the host to recognize a large number of pathogen-associated molecular patterns such as bacterial lipopolysaccharide, viral RNA, CpG-containing DNA and flagellin. Toll-like receptors have also been shown to play a pivotal role in both innate and adaptive immune responses. The role of Toll-like receptors as a primary part of our microbe defense system has been shown in several studies, but their possible function as mediators in allergy and asthma remains to be established. The present study was designed to examine the expression of Toll-like receptors 2, 3 and 4 in the nasal mucosa of patients with intermittent allergic rhinitis, focusing on changes induced by exposure to pollen. Methods: 27 healthy controls and 42 patients with seasonal allergic rhinitis volunteered for the study. Nasal biopsies were obtained before and during pollen season as well as before and after allergen challenge. The seasonal material was used for mRNA quantification of Toll-like receptors 2, 3 and 4 with real-time polymerase chain reaction, whereas specimens achieved in conjunction with allergen challenge were used for immunohistochemical localization and quantification of corresponding proteins. Results: mRNA and protein representing Toll-like receptors 2, 3 and 4 could be demonstrated in all specimens. An increase in protein expression for all three receptors could be seen following allergen challenge, whereas a significant increase of mRNA only could be obtained for Toll-like receptor 3 during pollen season. Conclusion: The up-regulation of Toll-like receptors 2, 3 and 4 in the nasal mucosa of patients with symptomatic allergic rhinitis supports the idea of a role for Toll-like receptors in allergic airway inflammation.
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页数:10
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共 33 条
[1]   STANDARDIZATION OF DIAGNOSTIC WORK IN ALLERGY [J].
AAS, K ;
BELIN, L .
INTERNATIONAL ARCHIVES OF ALLERGY AND APPLIED IMMUNOLOGY, 1973, 45 (1-2) :57-60
[2]   Expression of functional toll-like receptor-2 and-4 on alveolar epithelial cells [J].
Armstrong, L ;
Medford, ARL ;
Uppington, KM ;
Robertson, J ;
Witherden, IR ;
Tetley, TD ;
Millar, AB .
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, 2004, 31 (02) :241-245
[3]   IL-18 modulates chronic fungal asthma in a murine model; putative involvement of Toll-like receptor-2 [J].
Blease, K ;
Kunkel, SL ;
Hogaboam, CM .
INFLAMMATION RESEARCH, 2001, 50 (11) :552-560
[4]   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
[5]   Human β-defensins and toll-like receptors in the upper airway [J].
Claeys, S ;
de Belder, T ;
Holtappels, G ;
Gevaert, P ;
Verhasselt, B ;
van Cauwenberge, P ;
Bachert, C .
ALLERGY, 2003, 58 (08) :748-753
[6]   TLR-induced inflammation in cystic fibrosis and non-cystic fibrosis airway epithelial cells [J].
Greene, CM ;
Carroll, TP ;
Smith, SGJ ;
Taggart, CC ;
Devaney, J ;
Griffin, S ;
O'Neill, SJ ;
McElvaney, NG .
JOURNAL OF IMMUNOLOGY, 2005, 174 (03) :1638-1646
[7]   Response of human pulmonary epithelial cells to lipopolysaccharide involves Toll-like receptor 4 (TLR4)-dependent signaling pathways - Evidence for an intracellular compartmentalization of TLR4 [J].
Guillot, L ;
Medjane, S ;
Le-Barillec, K ;
Balloy, V ;
Danel, C ;
Chignard, M ;
Si-Tahar, M .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2004, 279 (04) :2712-2718
[8]   Toll-like receptors and their function in innate and adaptive immunity [J].
Heine, H ;
Lien, E .
INTERNATIONAL ARCHIVES OF ALLERGY AND IMMUNOLOGY, 2003, 130 (03) :180-192
[9]   Activation of toll-like receptor 2 on human tracheobronchial epithelial cells induces the antimicrobial peptide human β defensin-2 [J].
Hertz, CJ ;
Wu, Q ;
Porter, EM ;
Zhang, YJ ;
Weismüller, KH ;
Godowski, PJ ;
Ganz, T ;
Randell, SH ;
Modlin, RL .
JOURNAL OF IMMUNOLOGY, 2003, 171 (12) :6820-6826
[10]   Innate immune recognition [J].
Janeway, CA ;
Medzhitov, R .
ANNUAL REVIEW OF IMMUNOLOGY, 2002, 20 :197-216