ERJ
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Full Text (PDF)
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 PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Sano, T
Right arrow Articles by Ogura, T
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Sano, T
Right arrow Articles by Ogura, T
Eur Respir J 1995; 8: 1473-1478
Copyright © ERS Journals Ltd 1995


Original Articles

FK506 and cyclosporin A inhibit granulocyte/macrophage colony-stimulating factor production by mononuclear cells in asthma

T Sano, Y Nakamura, Y Matsunaga, T Takahashi, M Azuma, Y Okano, E Shimizu, F Ogushi, S Sone, and T Ogura

Bronchial asthma is associated with eosinophilic inflammation and expression of T-cell-derived cytokines, which influence eosinophilic function. FK506, a newly established immunosuppressive agent, may have potential as a therapeutic instrument for asthma because of its suppressive effect on T-cell activation. To assess this, we compared the inhibitory effects of FK506 and cyclosporin A on production of granulocyte/macrophage colony-stimulating factor and interleukin-5 by interleukin-2- or Dermatophagoides farinae-stimulated mononuclear cells from patients with asthma, and their contribution to proliferation and survival of eosinophils in vitro. FK506 inhibited granulocyte/macrophage colony-stimulating factor production by stimulated mononuclear cells from asthma patients at lower concentrations than cyclosporin A. Both drugs inhibited eosinophil proliferation and survival activity from mononuclear cells at comparable concentrations. Interleukin-5 production by stimulated mononuclear cells was also inhibited both by FK506 and cyclosporin A. We conclude that both FK506 and cyclosporin A have potential for therapy of bronchial asthma.


This article has been cited by other articles:


Home page
Am. J. Respir. Crit. Care Med.Home page
P. Borger, M. Tamm, J. L. Black, and M. Roth
Asthma: Is It Due to an Abnormal Airway Smooth Muscle Cell?
Am. J. Respir. Crit. Care Med., August 15, 2006; 174(4): 367 - 372.
[Abstract] [Full Text] [PDF]


Home page
ChestHome page
A. S. Niven and G. Argyros
Alternate Treatments in Asthma
Chest, April 1, 2003; 123(4): 1254 - 1265.
[Full Text] [PDF]


Home page
Am. J. Respir. Crit. Care Med.Home page
L. N. KHAN, O. M. KON, A. J. MACFARLANE, Q. MENG, S. YING, N. C. BARNES, and A. BARRY KAY
Attenuation of the Allergen-induced Late Asthmatic Reaction by Cyclosporin A Is Associated with Inhibition of Bronchial Eosinophils, Interleukin-5, Granulocyte Macrophage Colony-Stimulating Factor, and Eotaxin
Am. J. Respir. Crit. Care Med., October 1, 2000; 162(4): 1377 - 1382.
[Abstract] [Full Text] [PDF]


Home page
Drug Metab. Dispos.Home page
A. E. M. Vickers, R. M. Jimenez, M. C. Spaans, V. Pflimlin, R. L. Fisher, and K. Brendel
Human and Rat Lung Biotransformation of Cyclosporin A and Its Derivatives Using Slices and Bronchial Epithelial Cells
Drug Metab. Dispos., July 1, 1997; 25(7): 873 - 880.
[Abstract] [Full Text]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1995 by the European Respiratory Society.