| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
,
,¶
* Department of Biochemistry and Molecular Biology,
Department of Respiratory Medicine, and
Department of Pediatric Surgery, Faculty of Medicine, University of Tokyo, Tokyo, Japan;
Core Research for Evolutional Science and Technology and
¶ Precursory Research for Embryonic Science and Technology of Japan Science and Technology Agency, Kawaguchi, Japan; and
|| KOKORO Biology Group, Laboratories for Integrated Biology, Graduate School of Frontier Biosciences, Osaka University, Suita, Japan
Bronchial asthma is an increasingly common disorder that remains poorly understood and difficult to manage. The disease is characterized by airway hyperresponsiveness, chronic inflammation, and mucus overproduction. Based on the finding that leukotriene B4 receptor 1 (BLT1) is expressed highly in Th2 lymphocytes, we analyzed the roles of BLT1 using an OVA-induced bronchial asthma model. BLT1-null mice did not develop airway hyperresponsiveness, eosinophilic inflammation, and hyperplasia of goblet cells. Attenuated symptoms were accompanied by reduced IgE production, and accumulation of IL-5 and IL-13 in bronchoalveolar lavage fluid, suggesting attenuated Th2-type immune response in BLT1-null mice. Peribronchial lymph node cells of sensitized BLT1-null mice showed much attenuated proliferation and production of Th2 cytokines upon re-stimulation with Ag in vitro. Thus, LTB4-BLT1 axis is required for the development of Th2-type immune response, and blockade of LTB4 functions through BLT1 would be novel and useful in the effort to ameliorate bronchial asthma and related Th2-biased immune disorders.
This article has been cited by other articles:
|
|
 |
|
  N. Miyahara, H. Ohnishi, S. Miyahara, K. Takeda, S. Matsubara, H. Matsuda, M. Okamoto, J. E. Loader, A. Joetham, M. Tanimoto, et al. Leukotriene B4 Release from Mast Cells in IgE-Mediated Airway Hyperresponsiveness and Inflammation Am. J. Respir. Cell Mol. Biol., June 1, 2009; 40(6): 672 - 682. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N. Miyahara, H. Ohnishi, H. Matsuda, S. Miyahara, K. Takeda, T. Koya, S. Matsubara, M. Okamoto, A. Dakhama, B. Haribabu, et al. Leukotriene B4 Receptor 1 Expression on Dendritic Cells Is Required for the Development of Th2 Responses and Allergen-Induced Airway Hyperresponsiveness J. Immunol., July 15, 2008; 181(2): 1170 - 1178. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Okuno, Y. Iizuka, H. Okazaki, T. Yokomizo, R. Taguchi, and T. Shimizu 12(S)-hydroxyheptadeca-5Z, 8E, 10E-trienoic acid is a natural ligand for leukotriene B4 receptor 2 J. Exp. Med., April 14, 2008; 205(4): 759 - 766. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M.-R. Blanchet, S. Maltby, D. J. Haddon, H. Merkens, L. Zbytnuik, and K. M. McNagny CD34 facilitates the development of allergic asthma Blood, September 15, 2007; 110(6): 2005 - 2012. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. C. Fulkerson, C. A. Fischetti, M. L. McBride, L. M. Hassman, S. P. Hogan, and M. E. Rothenberg A central regulatory role for eosinophils and the eotaxin/CCR3 axis in chronic experimental allergic airway inflammation PNAS, October 31, 2006; 103(44): 16418 - 16423. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. C. Kim, F. I. Hsu, N. A. Barrett, D. S. Friend, R. Grenningloh, I-C. Ho, A. Al-Garawi, J. M. Lora, B. K. Lam, K. F. Austen, et al. Cysteinyl Leukotrienes Regulate Th2 Cell-Dependent Pulmonary Inflammation J. Immunol., April 1, 2006; 176(7): 4440 - 4448. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
