Skip Navigation

This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (5)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Nakata, A.
Right arrow Articles by Mori, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Nakata, A.
Right arrow Articles by Mori, A.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

International Immunology, Vol. 13, No. 3, 329-339, March 2001
© 2001 Japanese Society for Immunology

Correlation between eosinophilia induced by CD4+ T cells and bronchial hyper-responsiveness

Aya Nakata, Osamu Kaminuma, Koji Ogawa, Hisako Fujimura, Keiko Fushimi, Hideo Kikkawa, Kazuaki Naito, Katsuo Ikezawa, Robert W. Egan1, and Akio Mori2,

Discovery Research Laboratory, Tanabe Seiyaku Co., Ltd, 2-2-50 Kawagishi, Toda, Saitama 335-8505, Japan
1 Department of Allergy and Immunology, Schering-Plough Research Institute, 2015, Galloping Hill Road, Kenilworth, NJ 07033, USA
2 Clinical Research Laboratory for Allergy and Rheumatology, National Sagamihara Hospital, 18-1 Sakuradai, Sagamihara, Kanagawa 228-8522, Japan

Correspondence to: A. Nakata

The relationship between CD4+ T cell-mediated airway eosinophilic inflammation and bronchial hyper-responsiveness (BHR) was investigated. Ovalbumin-reactive Th0 clones were adoptively transferred to unprimed BALB/c mice and then the mice were challenged by inhalation of the relevant antigen. Upon antigen provocation, infused Th clones infiltrated into the airways, followed by the accumulation and degranulation of eosinophils, goblet cell hyperplasia, edema and increase in bronchial responsiveness to acetylcholine. Transfer of several clones that differed in the levels of IL-5 production revealed that the magnitude of in vivo eosinophilia strongly correlated with the IL-5-producing capacity of the infused Th clones. Administration of anti-IL-5 mAb almost completely suppressed antigen-induced eosinophilic inflammation and BHR. Administration of anti-IL-4 mAb or anti-IFN-{gamma} mAb enhanced the eosinophilia and BHR, whereas anti-IL-2 mAb did not affect them. The number of accumulated eosinophils significantly correlated with the intensity of BHR. Our present results clearly demonstrated that CD4+ T cells induced BHR as a result of eosinophilic inflammation. IL-5 totally regulated both responses.

Keywords: cytokines, eosinophils, in vivo animal models, lung, T lymphocytes

Transmitting editor: K. Takatsu


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Int ImmunolHome page
A. Mori, K. Ogawa, K. Someya, Y. Kunori, D. Nagakubo, O. Yoshie, F. Kitamura, T. Hiroi, and O. Kaminuma
Selective suppression of Th2-mediated airway eosinophil infiltration by low-molecular weight CCR3 antagonists
Int. Immunol., August 1, 2007; 19(8): 913 - 921.
[Abstract] [Full Text] [PDF]

Home page
 Proc Am Thorac SocHome page
D. C. Grootendorst and K. F. Rabe
Mechanisms of Bronchial Hyperreactivity in Asthma and Chronic Obstructive Pulmonary Disease
Proceedings of the ATS, April 1, 2004; 1(2): 77 - 87.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.