| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Department of Biology, Hong Kong University of Science and Technology, Hong Kong, People’s Republic of China
In the airway epithelia, extracellular adenosine modulates a number of biological processes. However, little is known about adenosine’s role in the inflammatory responses of airway epithelial cells. Recent studies suggest that the chronic elevation of extracellular adenosine in mice leads to pulmonary inflammation and fibrosis. Yet, the underlying molecular mechanism has not been well understood and little attention has been paid to the role of airway epithelia in adenosine-triggered inflammation. In the present work, we examined the role of adenosine in releasing IL-6 from airway epithelia. In Calu-3 human airway epithelial cells, apical but not basolateral adenosine elicited robust, apically polarized release of IL-6, along with proinflammatory IL-8. Both protein kinase A and protein kinase C mediated the adenosine-induced IL-6 release, at least partly via phosphorylation of CREB. Protein kinase C appeared to phosphorylate CREB through activating ERK. In addition, A2A but not A2B adenosine receptors were specifically required for the adenosine-induced IL-6 release. Furthermore, in rat bronchoalveolar lavage fluid, adenosine triggered the release of IL-6 as well as proinflammatory IL-1β. Adenosine also mediated the release of a considerable portion of the LPS-induced IL-6 in rat bronchoalveolar lavage fluid. Our findings provide a possible molecular link between extracellular adenosine elevation and lung inflammation and fibrosis.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 This work was supported by Hong Kong Research Grants Council Grants HKUST6275/03M and HKUST6468/05M. F.W. was supported by postdoctoral matching funds from the Hong Kong University of Science and Technology.
2 Y.S. and F.W. contributed equally to this work.
3 Address correspondence and reprint requests to Dr. Pingbo Huang, Department of Biology, Hong Kong University of Science and Technology, Clear Water Bay, Kowloon, Hong Kong, People’s Republic of China. E-mail address: bohuangp{at}ust.hk
4 Abbreviations used in this paper: BAL, bronchoalveolar lavage; BIM, bisindolylmaleimide; BALF, BAL fluid; DPCPX, 1,3-dipropyl-8-cyclopentylxanthine; NECA, 5'-N-ethylcarboxamidoadenosine; PKA, protein kinase A; PKC, protein kinase C; PLC, phospholipase C; siRNA, small interfering RNA; 8-SPT, 8-(p- sulfophenyl)theophylline.
This article has been cited by other articles:
|
|
 |
|
  E. Theatre, V. Bours, and C. Oury A P2X Ion Channel-Triggered NF-{kappa}B Pathway Enhances TNF-{alpha}-Induced IL-8 Expression in Airway Epithelial Cells Am. J. Respir. Cell Mol. Biol., December 1, 2009; 41(6): 705 - 713. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y. Zhou, A. Mohsenin, E. Morschl, H. W. J. Young, J. G. Molina, W. Ma, C.-X. Sun, H. Martinez-Valdez, and M. R. Blackburn Enhanced Airway Inflammation and Remodeling in Adenosine Deaminase-Deficient Mice Lacking the A2B Adenosine Receptor J. Immunol., June 15, 2009; 182(12): 8037 - 8046. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
