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Lipopolysaccharide Stimulation of the Human Neutrophil*: An Analysis of Changes in Gene Transcription and Protein Expression by Oligonucleotide Microarrays and Proteomics

Michael B. Fessler, MD; Kenneth C. Malcolm, PhD; Mark William Duncan, PhD; G. Scott Worthen, MD
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*From the Departments of Medicine of National Jewish Medical and Research Center and University of Colorado Health Sciences Center; Biochemical Mass Spectrometry Facility, University of Colorado Health Sciences Center, Denver, CO.

Correspondence to: Michael Fessler, MD, Biochemical Mass Spectrometry Facility, Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado Health Sciences Center, 4200 E 9th Ave, Box C272, Denver, CO 80262; e-mail: fesslerm@njc.org



Chest. 2002;121(3_suppl):75S-76S. doi:10.1378/chest.121.3_suppl.75S
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Bacterial lipopolysaccharide (LPS) evokes several functional responses in the polymorphonuclear leukocyte (PMN) that contribute to innate immunity. While certain responses, such as adhesion and synthesis of tumor necrosis factor-α, are inhibited by pretreatment with an inhibitor of p38 mitogen-activated protein kinase (MAPk), others, such as actin assembly, are unaffected. The aim of the present study was to investigate the changes in PMN gene transcription and protein expression following LPS exposure and their dependence on p38 MAPk signaling.

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