Der p2 Activates Airway Smooth Muscle Cells in a TLR2/MyD88-Dependent Manner to Induce an Inflammatory Response

被引:70
作者
Chiou, Ya-Ling [2 ]
Lin, Ching-Yuang [1 ,2 ]
机构
[1] China Med Univ, China Med Univ Hosp, Grad Inst Clin Med Sci, Taichung 40402, Taiwan
[2] Natl Yang Ming Univ, Inst Microbiol & Immunol, Taipei 112, Taiwan
关键词
TOLL-LIKE RECEPTORS; HOUSE-DUST MITE; DENDRITIC CELLS; IMMUNE-RESPONSE; PROTEIN-KINASE; CUTTING EDGE; EXPRESSION; ASTHMA; ALLERGEN; AGONISTS;
D O I
10.1002/jcp.21764
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Der p2 is a major allergen from Dermatophagoides pteronyssinus, the main species of house dust mite and a major inducer of asthma, inducing harmful respiratory inflammatory responses by activating cells in the respiratory tract, leading to an unstable status. We hypothesize that Der p2 may induce local inflammatory responses by directly affecting airway smooth muscle (ASM) cells. In this study, we demonstrated that Der p2 raised nuclear factor-kappa B (NF-kappa B) and extracellular signal-regulated kinase (ERK) 1/2 activation and induced a high level of proinflammatory cytokines expression in primary cultured ASM cells. Der p2 activated the MyD88 signaling pathway through toll-like receptor (TLR) 2, not through TLR4. Notably, Der p2 stimulated ASM cells to increase phosphorylation of ERK 1/2 and expression of c-Fos, which were also important in the T helper type 2 (Th2) immune response. These results suggest that Der p2 induces asthma through the MyD88 signaling pathway in respiratory tissue. J. Cell. Physiol. 220: 311-318, 2009. (C) 2009 Wiley-Liss, Inc.
引用
收藏
页码:311 / 318
页数:8
相关论文
共 52 条
[1]   Cutting edge: Different toll-like receptor agonists instruct dendritic cells to induce distinct th responses via differential modulation of extracellular signal-regulated kinase-mitogen-activated protein kinase and c-fos [J].
Agrawal, S ;
Agrawal, A ;
Doughty, B ;
Gerwitz, A ;
Blenis, J ;
Van Dyke, T ;
Pulendran, B .
JOURNAL OF IMMUNOLOGY, 2003, 171 (10) :4984-4989
[2]   Pathogen recognition and innate immunity [J].
Akira, S ;
Uematsu, S ;
Takeuchi, O .
CELL, 2006, 124 (04) :783-801
[3]  
Becker A, 2000, ANN NY ACAD SCI, V921, P275
[4]   Genetic analysis of host resistance: Toll-like receptor signaling and immunity at large [J].
Beutler, Bruce ;
Jiang, Zhengfan ;
Georgel, Philippe ;
Crozat, Karine ;
Croker, Ben ;
Rutschmann, Sophie ;
Du, Xin ;
Hoebe, Kasper .
ANNUAL REVIEW OF IMMUNOLOGY, 2006, 24 :353-389
[5]   Intranasal and inhaled fluticasone propionate for pollen-induced rhinitis and asthma [J].
Dahl, R ;
Nielsen, LP ;
Kips, J ;
Foresi, A ;
van Cauwenberge, P ;
Tudoric, N ;
Howarth, P ;
Richards, DH ;
Williams, M ;
Pauwels, R .
ALLERGY, 2005, 60 (07) :875-881
[6]   The link between fungi and severe asthma: a summary of the evidence [J].
Denning, DW ;
O'Driscoll, BR ;
Hogaboam, CM ;
Bowyer, P ;
Niven, RM .
EUROPEAN RESPIRATORY JOURNAL, 2006, 27 (03) :615-626
[7]   Flagellin promotes myeloid differentiation factor 88-dependent development of Th2-type response [J].
Didierlaurent, A ;
Ferrero, I ;
Otten, LA ;
Dubois, B ;
Reinhardt, M ;
Carlsen, H ;
Blomhoff, R ;
Akira, S ;
Kraehenbuhl, JP ;
Sirard, JC .
JOURNAL OF IMMUNOLOGY, 2004, 172 (11) :6922-6930
[8]   Pathological role of IL-6 in the experimental allergic bronchial asthma in mice [J].
Doganci, A ;
Sauer, K ;
Karwot, R ;
Finotto, S .
CLINICAL REVIEWS IN ALLERGY & IMMUNOLOGY, 2005, 28 (03) :257-269
[9]   Lipopolysaccharide-enhanced, toll-like receptor 4-dependent T helper cell type 2 responses to inhaled antigen [J].
Eisenbarth, SC ;
Piggott, DA ;
Huleatt, JW ;
Visintin, I ;
Herrick, CA ;
Bottomly, K .
JOURNAL OF EXPERIMENTAL MEDICINE, 2002, 196 (12) :1645-1651
[10]   Mal (MyD88-adapter-like) is required for Toll-like receptor-4 signal transduction [J].
Fitzgerald, KA ;
Palsson-McDermott, EM ;
Bowie, AG ;
Jefferies, CA ;
Mansell, AS ;
Brady, G ;
Brint, E ;
Dunne, A ;
Gray, P ;
Harte, MT ;
McMurray, D ;
Smith, DE ;
Sims, JE ;
Bird, TA ;
O'Neill, LAJ .
NATURE, 2001, 413 (6851) :78-83