Der p2 activates airway smooth muscle cells in a TLR2/MyD88-dependent manner to induce an inflammatory response
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 lo...
Saved in:
Published in | Journal of cellular physiology Vol. 220; no. 2; pp. 311 - 318 |
---|---|
Main Authors | , |
Format | Journal Article |
Language | English |
Published |
Hoboken
Wiley Subscription Services, Inc., A Wiley Company
01.08.2009
|
Subjects | |
Online Access | Get full text |
Cover
Loading…
Summary: | 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‐κB) 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 ERK1/2 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. © 2009 Wiley‐Liss, Inc. |
---|---|
Bibliography: | All contributing authors declared no conflicts of interest to disclose, whether financial or of any other nature. istex:40E4168494ADF5805BA2C9D658FF40C3CFA84776 ark:/67375/WNG-JFLBCF48-C ArticleID:JCP21764 ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0021-9541 1097-4652 |
DOI: | 10.1002/jcp.21764 |