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An Intracellular Signaling Pathway Linking Lipopolysaccharide Stimulation to Cellular Responses of the Human Neutrophil*: The p38 MAP Kinase Cascade and its Functional Significance

Jerry A. Nick, MD; Natalie J. Avdi; Scott K. Young; Patrick P. McDonald, PhD; Marcella A. Billstrom, PhD; Peter M. Henson, PhD; Gary L. Johnson, PhD; G. Scott Worthen, MD
Author and Funding Information

*From the Department of Medicine (Drs. Nick, Avdi, Young, Billstrom, and Worthen), Department of Pediatrics (Drs. McDonald and Henson), Division of Basic Sciences (Dr. Johnson), and Program in Molecular Signal Transduction (Drs. Johnson and Worthen), National Jewish Medical and Research Center, Denver, CO; and the Departments of Medicine (Drs. Nick, Henson, and Worthen) and Pharmacology (Dr. Johnson), University of Colorado School of Medicine, Denver, CO.

Correspondence to: Jerry A. Nick, MD, National Jewish Medical and Research Center, 1400 Jackson St, Denver, CO 80206; e-mail: nickj@njc.org



Chest. 1999;116(suppl_1):54S-55S. doi:10.1378/chest.116.suppl_1.54S
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Activation and accumulation of neutrophils in the lung by proinflammatory stimuli is a central event in the pathogenesis of ARDS. Following exposure of the neutrophil to a stimulus, sequential phosphorylation of kinases creates an intracellular signal that results in specific functional responses. Integral to many intracellular signaling pathways is activation of a three-part mitogen-activated protein (MAP) kinase cascade. MAP kinases (MAPk) are a highly conserved superfamily that are central to the regulation of cell growth, differentiation, and stress responses.1 At least three distinct families of MAPks exist in mammalian cells: the p42/44 extracellular signal-regulated kinase (ERK) MAPks,2 c-Jun NH2-terminal kinases,3 and the p38 MAPk.4 Stimulation of human neutrophils with lipopolysaccharide (LPS) has been shown to result in the phosphorylation and activation of the p38 MAP kinase (MAPk), but not the p42/44 MAPks or the c-Jun NH2-terminal MAPk.7 The goal of this study is to expand our knowledge of the intracellular signaling pathway utilized by the neutrophil in response to LPS by addressing two fundamental questions: what upstream kinase activates p38 MAPk, and what are the functional consequences of this activation?


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