| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Department of Thoracic Medicine, Imperial College School of Medicine at the National Heart and Lung Institute, London SW3 6LY, United Kingdom
Epithelial cells play a critical role in airway inflammation and have the capacity to produce many inflammatory mediators, including bioactive lipids and proinflammatory cytokines. Intracellular levels of cAMP and cGMP are important in the control of inflammatory cell function. These cyclic nucleotides are inactivated via a family of phosphodiesterase (PDE) enzymes, providing a possible site for drug intervention in chronic inflammatory conditions. We studied the expression of PDE activity in an epithelial cell line (A549) and in primary human airway epithelial cells (HAECs). We measured PDE function using specific inhibitors to identify the PDE families present and used RT-PCR to elucidate the expression of PDE isogenes. Both A549 cells and HAECs predominantly expressed PDE4 activity, with lesser PDE1, PDE3, and PDE5 activity. RT-PCR identified HSPDE4A5 and HSPDE4D3 together with HSPDE7. Inhibition of PDE4 and PDE3 reduced secretion by these cells. Epithelial PDE may be an important target for PDE4 inhibitors in the development of the control of asthmatic inflammation, particularly when delivered via the inhaled route.
phosphodiesterase type 3; phosphodiesterase type 4; inflammation; granulocyte-macrophage colony-stimulating factor; airway epithelial cells
This article has been cited by other articles:
|
|
 |
|
  H. Mori, T. Nose, K. Ishitani, S. Kasagi, S. Souma, T. Akiyoshi, Y. Kodama, T. Mori, M. Kondo, S. Sasaki, et al. Phosphodiesterase 4 inhibitor GPD-1116 markedly attenuates the development of cigarette smoke-induced emphysema in senescence-accelerated mice P1 strain Am J Physiol Lung Cell Mol Physiol, February 1, 2008; 294(2): L196 - L204. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Draheim, U. Egerland, and C. Rundfeldt Anti-Inflammatory Potential of the Selective Phosphodiesterase 4 Inhibitor N-(3,5-Dichloro-pyrid-4-yl)-[1-(4-fluorobenzyl)-5-hydroxy-indole-3-yl]-glyoxylic Acid Amide (AWD 12-281), in Human Cell Preparations J. Pharmacol. Exp. Ther., February 1, 2004; 308(2): 555 - 563. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. B. Tarpey, D. R. Sawmiller, C. Kelly, W. J. Thompson, and M. I. Townsley Phosphodiesterase 3 activity is reduced in dog lung following pacing-induced heart failure Am J Physiol Lung Cell Mol Physiol, May 1, 2003; 284(5): L766 - L773. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. J. Smith, S. Brookes-Fazakerley, L. E. Donnelly, P. J. Barnes, M. S. Barnette, and M. A. Giembycz Ubiquitous expression of phosphodiesterase 7A in human proinflammatory and immune cells Am J Physiol Lung Cell Mol Physiol, February 1, 2003; 284(2): L279 - L289. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Kohyama, X. Liu, Y. K. Zhu, F.-Q. Wen, H. J. Wang, Q. Fang, T. Kobayashi, and S. I. Rennard Phosphodiesterase 4 Inhibitor Cilomilast Inhibits Fibroblast-Mediated Collagen Gel Degradation Induced by Tumor Necrosis Factor-{alpha} and Neutrophil Elastase Am. J. Respir. Cell Mol. Biol., October 1, 2002; 27(4): 487 - 494. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. Ito, E. Jazrawi, B. Cosio, P. J. Barnes, and I. M. Adcock p65-activated Histone Acetyltransferase Activity Is Repressed by Glucocorticoids. MIFEPRISTONE FAILS TO RECRUIT HDAC2 TO THE p65-HAT COMPLEX J. Biol. Chem., August 3, 2001; 276(32): 30208 - 30215. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
