Anti-interleukin 8 autoantibody:interleukin 8 immune complexes visualized by laser confocal microscopy in injured lung.
Abstract
Anti-interleukin 8 autoantibody:interleukin 8 (anti-IL-8 autoantibody:IL-8) complexes are present in lung fluids of patients with acute lung injury/acute respiratory distress syndrome (ALI/ARDS), and levels of these complexes correlate with progression to and the outcome of ARDS. Fc gammaRIIa, an immunoglobulin G (IgG) receptor, mediates proinflammatory activity of the complexes.
To evaluate lung tissues from patients with ARDS for presence of anti-IL-8 autoantibody:IL-8 complexes and to establish whether the complexes associate with Fc gammaRIIa.
Lung tissue sections from 3 patients with ARDS and sections of normal lung tissues from 3 patients were stained with antibodies against IL-8 and IgG to detect immune complexes and with antibody against Fc gammaRIIa. In some experiments, sections were blocked with anti-Fc gamma RIIa antibody before staining. Samples were analyzed using confocal microscopy.
Interleukin 8 costained with IgG and Fc gammaRIIa in lung tissues from patients with ARDS but not in control tissues, suggesting that anti-IL-8 autoantibody:IL-8 complexes are deposited in lungs of patients with ARDS via Fc gammaRIIa. Further, colocalization between IL-8 and Fc gammaRIIa could be blocked by anti-Fc gammaRIIa.
Our data demonstrate that anti-IL-8 autoantibody:IL-8 complexes are present in lung tissues of patients with ARDS, and are attached to Fc gammaRIIa.
To evaluate lung tissues from patients with ARDS for presence of anti-IL-8 autoantibody:IL-8 complexes and to establish whether the complexes associate with Fc gammaRIIa.
Lung tissue sections from 3 patients with ARDS and sections of normal lung tissues from 3 patients were stained with antibodies against IL-8 and IgG to detect immune complexes and with antibody against Fc gammaRIIa. In some experiments, sections were blocked with anti-Fc gamma RIIa antibody before staining. Samples were analyzed using confocal microscopy.
Interleukin 8 costained with IgG and Fc gammaRIIa in lung tissues from patients with ARDS but not in control tissues, suggesting that anti-IL-8 autoantibody:IL-8 complexes are deposited in lungs of patients with ARDS via Fc gammaRIIa. Further, colocalization between IL-8 and Fc gammaRIIa could be blocked by anti-Fc gammaRIIa.
Our data demonstrate that anti-IL-8 autoantibody:IL-8 complexes are present in lung tissues of patients with ARDS, and are attached to Fc gammaRIIa.
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