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1 Department of Biochemistry, University of Texas Health Center, Tyler, TX, USA
2 Cardiovascular Research Institute, University of California, San Francisco, CA, USA
* To whom correspondence should be addressed. E-mail: anna.kurdowska{at}uthct.edu.
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 (MPO) 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.
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