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Am. J. Respir. Cell Mol. Biol., Volume 21, Number 3, September, 1999 388-394

Interleukin-1 Receptor Antagonist Inhibits Interleukin-8 Expression in A549 Respiratory Epithelial Cells Infected In Vitro with a Replication-Deficient Recombinant Adenovirus Vector

Yehuda A. Schwarz, Raouf S. Amin, James M. Stark, Bruce C. Trapnell, and Robert W. Wilmott

Division of Pulmonary Medicine, Tel-Aviv Sourasky Medical Center, Tel Aviv, Israel; Division of Pulmonary Medicine, Children's Hospital Medical Center, Cincinnati, Ohio; and Department of Virology, Genetic Therapy, Inc., Gaithersburg, Maryland

In an earlier study, we showed that a recombinant adenovirus vector with deletions in the E1 and E3 regions of the viral genome (AV1LacZ4) induces expression of interleukin (IL)-8 in A549 cells (a human respiratory cell line). IL-8 can be induced through several pathways, including activation by IL-1. We tested the hypothesis that the induction of IL-8 by the AV1LacZ4 adenovirus is accomplished by means of the IL-1/IL-8 activation pathway, which could be blocked by IL-1 receptor antagonist (IRAP). Viral infections of A549 cells were performed at a multiplicity of infection (MOI) of 50 in the presence and absence of IRAP (50 ng/ml). A549 cells were also stimulated with tumor necrosis factor (TNF)-alpha (100 ng/ml), a known stimulant of IL-8, in the presence and absence of IRAP. IL-8 expression was evaluated by Northern blot analysis and enzyme-linked immunosorbent assay. Levels of IL-8 protein and messenger RNA (mRNA) were greater in the infected cells than in the uninfected ones at 24, 48, and 96 h (P < 0.01). Virus-infected cells treated with IRAP expressed 75% less IL-8 mRNA and protein (P < 0.01) than did untreated cells, whereas IRAP pretreatment of TNF-alpha -stimulated cells did not affect IL-8 production. IL-1 production by the virus-infected cells was detectable by concentration of the supernatants and reverse transcription-polymerase chain reaction. We conclude that IL-8 is produced by virus vector-infected cells, partly through IL-1 activation that can be downregulated by IRAP.




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Proc. Am. Thorac. Soc. Am. J. Respir. Crit. Care Med.
Copyright © 1999 American Thoracic Society.