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Anti-IL-8 Autoantibodies in Alveolar Fluid From Patients at Risk for ARDS and With Well-defined ARDS* FREE TO VIEW

A. Kurdowska, PhD; J.M. Noble; K.P. Steinberg, MD, FCCP; J. Ruzinski; L.D. Hudson, MD, FCCP; T.R. Martin, MD, FCCP
Author and Funding Information

*From the University of Texas Health Center, Tyler, TX, and Seattle Veterans Affairs Medical Center and Department of Pulmonary/Critical Care Medicine, Harborview Medical Center, Seattle, WA. This work was supported by the NIH grant 1R29HL56768 and HL30542.

Correspondence to: Anna Kurdowska, PhD, Dept of Biochemistry, Univ Texas Health Ctr, 11937 US Hwy 271, Tyler, TX 75708-3154

Chest. 1999;116(suppl_1):9S. doi:10.1378/chest.116.suppl_1.9S
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The accumulation and degranulation of neutrophils (polymorphonuclear leukocytes [PMNs]) may contribute to severe lung injury in patients with ARDS. Interleukin-8 (IL-8), a potent neutrophil attractant and activator, has been implicated in the PMN recruitment. Due to increased epithelial and endothelial permeability, which occurs in association with ARDS, higher-molecular-weight proteins, such as IgG and IgM, enter airspaces. Our previous studies show that a significant portion of IL-8 in lung fluids from patients with ARDS is associated with anti-IL-8 autoantibodies (anti-IL-8:IL-8 complexes). In addition, our earlier findings suggest that these autoantibodies to IL-8 may be important in controlling IL-8 function by neutralizing its biological activity and/or facilitating clearance of IL-8 by the reticuloendothelial system. To further define the function of these autoantibodies in ARDS patients, we measured concentrations of free and complexed IL-8 in BAL fluids from 19 patients at risk for ARDS and 40 patients with well-defined ARDS (1, 3, 7, 14, and 21 days after the onset of ARDS). Patients at risk for ARDS had less anti-IL-8:IL-8 complexes than patients with ARDS (day 1). In ARDS, the highest concentration occurred in patients who died, and the concentrations did not decline with time. In contrast, in survivors, the concentrations were significantly lower and declined with time. The increased amount of anti-IL-8:IL-8 complexes was associated with the development of ARDS in patients at risk and death in patients with ARDS. Both free IL-8 and anti-IL-8:IL-8 complexes correlated with concentrations of PMNs (p < 0.05; r2 = 0.60 and 0.30, respectively) in patients at risk for ARDS. In ARDS patients, anti-IL-8:IL-8 complexes correlated with PMNs on day 3, whereas free IL-8 correlated with PMNs on days 3, 7, and 14.

This study indicates that the autoantibodies might contribute to the inflammatory process in ARDS. The elevated concentration of the complexes related to the severity of ARDS suggests that anti-IL-8 autoantibodies may also act as IL-8 carrier and enhance its activity. Our data show that the balance between free and complexed IL-8 needs to be considered in assessing the function of IL-8 in patients with ARDS.




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