| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Department of Molecular Biology, University of Texas Health Center at Tyler, Tyler, Texas 75708-3154
Submitted 6 May 2004 ; accepted in final form 21 May 2004
Interleukin (IL)-8, a C-X-C chemokine, is a potent chemoattractant and an activator for neutrophils, T cells, and other immune cells. The airway and respiratory epithelia play important roles in the initiation and modulation of inflammatory responses via production of cytokines and surfactant. The association between elevated levels of nitric oxide (NO) and IL-8 in acute lung injury associated with sepsis, acute respiratory distress syndrome, respiratory syncytial virus infection in infants, and other inflammatory diseases suggested that NO may play important roles in the control of IL-8 gene expression in the lung. We investigated the role of NO in the control of IL-8 gene expression in H441 lung epithelial cells. We found that a variety of NO donors significantly induced IL-8 mRNA levels, and the increase in IL-8 mRNA was associated with an increase in IL-8 protein. NO induction of IL-8 mRNA was due to increases in IL-8 gene transcription and mRNA stability. NO induction of IL-8 mRNA levels was not inhibited by 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one and KT-5823, inhibitors of soluble guanylate cyclase and protein kinase G, respectively, and 8-bromo-cGMP did not increase IL-8 mRNA levels. This indicated that NO induces IL-8 mRNA levels independently of changes in the intracellular cGMP levels. NO induction of IL-8 mRNA was significantly reduced by inhibitors of extracellular regulated kinase and protein kinase C. IL-8 induction by NO was also reduced by hydroxyl radical scavengers such as dimethyl sulfoxide and dimethylthiourea, indicating the involvement of hydroxyl radicals in the induction process. NO induction of IL-8 gene expression could be a significant contributing factor in the initiation and induction of inflammatory response in the respiratory epithelium.
inflammation; lung injury; respiratory epithelium; oxidants
This article has been cited by other articles:
|
|
 |
|
  C. L. Quement, I. Guenon, J.-Y. Gillon, V. Lagente, and E. Boichot MMP-12 induces IL-8/CXCL8 secretion through EGFR and ERK1/2 activation in epithelial cells Am J Physiol Lung Cell Mol Physiol, June 1, 2008; 294(6): L1076 - L1084. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. L. Ballard, J. D. Merrill, W. E. Truog, R. I. Godinez, M. H. Godinez, T. M. McDevitt, Y. Ning, S. G. Golombek, L. A. Parton, X. Luan, et al. Surfactant Function and Composition in Premature Infants Treated With Inhaled Nitric Oxide Pediatrics, August 1, 2007; 120(2): 346 - 353. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Das and V. Boggaram Proteasome dysfunction inhibits surfactant protein gene expression in lung epithelial cells: mechanism of inhibition of SP-B gene expression Am J Physiol Lung Cell Mol Physiol, January 1, 2007; 292(1): L74 - L84. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
I. Kuwahara, E. P. Lillehoj, W. Lu, I. S. Singh, Y. Isohama, T. Miyata, and K. C. Kim Neutrophil elastase induces IL-8 gene transcription and protein release through p38/NF-{kappa}B activation via EGFR transactivation in a lung epithelial cell line Am J Physiol Lung Cell Mol Physiol, September 1, 2006; 291(3): L407 - L416. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. J. M. Openshaw and J. S. Tregoning Immune Responses and Disease Enhancement during Respiratory Syncytial Virus Infection Clin. Microbiol. Rev., July 1, 2005; 18(3): 541 - 555. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
