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Am J Physiol Lung Cell Mol Physiol (December 21, 2001). doi:10.1152/ajplung.00378.2001
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Articles in PresS, published online ahead of print December 20, 2001
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00378.2001
Submitted on September 24, 2001
Accepted on December 15, 2001

Activity of pulmonary edema fluid interleukin-8 boundto {alpha}2-macroglobulin in patients with acute lung injury

Anna K Kurdowska1*, Thomas K Geiser2, Susanne M Alden1, Bozena R Dziadek1, James M Noble1, Thomas J Nuckton2, and Michael A Matthay2

1 Biochemistry, University of Texas Health Center at Tyler, Tyler, TX, USA
2 Cardiovascular Research Institute, University of California, School of Medicine, San Francisco, CA, USA

* To whom correspondence should be addressed. E-mail: anna.kurdowska{at}uthct.edu.

The formation of {alpha}2-macroglobulin ({alpha}2-M):interleukin-8 (IL-8) complexes may influence the biological activity of IL-8 and the quantitative assessment of IL-8 activity. Therefore, in this study, concentrations of free IL-8 and IL-8 complexes with {alpha}2-M were measured in pulmonary edema fluid samples from patients with the acute lung injury/acute respiratory distress syndrome (ALI/ARDS) and compared to control patients with hydrostatic pulmonary edema. Patients with ALI/ARDS had significantly higher concentrations of {alpha}2-M (p<0.01) as well as {alpha}2-M:IL-8 complexes (p<0.05). Because a substantial amount of IL-8 is complexed to {alpha}2-M, standard assays of free IL-8 may significantly underestimate the concentration of biologically active IL-8 in the distal airspaces of patients with ALI/ARDS. Furthermore, IL-8 bound to {alpha}2-M retained its biological activity, and this fraction of IL-8 was protected from proteolytic degradation. Thus, complex formation may modulate the acute inflammatory process in the lung.




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