| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
TRANSLATIONAL PHYSIOLOGY
Acute Lung Injury
1Department of Biochemistry, University of Texas Health Center, Tyler, Texas 75708; and 2School of Medicine, Cardiovascular Research Institute, University of California, San Francisco, California 94143-0130
Submitted 15 August 2003 ; accepted in final form 30 December 2003
A significant fraction of IL-8 in lung fluids from patients with the acute lung injury (ALI) is associated with anti-IL-8 autoantibodies (anti-IL-8:IL-8 complexes), and lung fluid concentrations of these complexes correlate with development and outcome of ALI. In this study, we examined whether anti-IL-8:IL-8 complexes exhibit proinflammatory activity in vitro. These complexes were purified from pulmonary edema fluid samples obtained from patients with ALI. First, we found that IL-8 bound to the autoantibody retained its ability to trigger chemotaxis of neutrophils, whereas control antibody did not have significant chemotactic activity. Next, we examined the ability of anti-IL-8:IL-8 complexes to induce neutrophil activation, i.e., neutrophil respiratory burst and degranulation. Anti-IL-8:IL-8 complexes triggered superoxide and myeloperoxidase release from human neutrophils, and in contrast, the control antibody had no effect. We also demonstrated that IgG receptor, Fc
RIIa, is the receptor involved in cellular activation mediated by these complexes. Blockade of FcRIIa completely reverses activity of the complexes with the exception of chemotaxis. Both FcRIIa and IL-8 receptors mediate chemotactic activity of anti-IL-8:IL-8 complexes, with FcRIIa being, however, a predominant receptor. Furthermore, activity of the complexes is partially dependent on the activation of the mitogen-activated protein kinases, i.e., ERK and p38, important components of the FcRIIa signaling cascade. Anti-IL-8:IL-8 complexes may therefore be involved in the pathogenesis of lung inflammation in clinical acute lung injury.
anti-IL-8:IL-8 complexes in pulmonary edema fluid; neutrophils; IgG receptors; neutrophil activation; mitogen-activated protein kinases
This article has been cited by other articles:
|
|
 |
|
  I. Parastatidis, L. Thomson, D. M. Fries, R. E. Moore, J. Tohyama, X. Fu, S. L. Hazen, H. F.G. Heijnen, M. K. Dennehy, D. C. Liebler, et al. Increased Protein Nitration Burden in the Atherosclerotic Lesions and Plasma of Apolipoprotein A-I Deficient Mice Circ. Res., August 17, 2007; 101(4): 368 - 376. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Fudala, A. Krupa, M. A. Matthay, T. C. Allen, and A. K. Kurdowska Anti-IL-8 autoantibody:IL-8 immune complexes suppress spontaneous apoptosis of neutrophils Am J Physiol Lung Cell Mol Physiol, August 1, 2007; 293(2): L364 - L374. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Reutershan, R. Stockton, A. Zarbock, G. W. Sullivan, D. Chang, D. Scott, M. A. Schwartz, and K. Ley Blocking p21-activated Kinase Reduces Lipopolysaccharide-induced Acute Lung Injury by Preventing Polymorphonuclear Leukocyte Infiltration Am. J. Respir. Crit. Care Med., May 15, 2007; 175(10): 1027 - 1035. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. Thomson, J. Christie, C. Vadseth, P. N. Lanken, X. Fu, S. L. Hazen, and H. Ischiropoulos Identification of Immunoglobulins that Recognize 3-Nitrotyrosine in Patients with Acute Lung Injury after Major Trauma Am. J. Respir. Cell Mol. Biol., February 1, 2007; 36(2): 152 - 157. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. E. Parsons Bridging the chasm between bench and bedside: translational research in acute lung injury Am J Physiol Lung Cell Mol Physiol, June 1, 2004; 286(6): L1086 - L1087. [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
