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Research Article Free access | 10.1172/JCI949

Neutrophils exposed to bacterial lipopolysaccharide upregulate NADPH oxidase assembly.

F R DeLeo, J Renee, S McCormick, M Nakamura, M Apicella, J P Weiss, and W M Nauseef

Department of Medicine and the Inflammation Program, Veterans Administration Medical Center and University of Iowa, Iowa City, Iowa 52246, USA.

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Department of Medicine and the Inflammation Program, Veterans Administration Medical Center and University of Iowa, Iowa City, Iowa 52246, USA.

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Department of Medicine and the Inflammation Program, Veterans Administration Medical Center and University of Iowa, Iowa City, Iowa 52246, USA.

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Department of Medicine and the Inflammation Program, Veterans Administration Medical Center and University of Iowa, Iowa City, Iowa 52246, USA.

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Department of Medicine and the Inflammation Program, Veterans Administration Medical Center and University of Iowa, Iowa City, Iowa 52246, USA.

Find articles by Apicella, M. in: PubMed | Google Scholar

Department of Medicine and the Inflammation Program, Veterans Administration Medical Center and University of Iowa, Iowa City, Iowa 52246, USA.

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Department of Medicine and the Inflammation Program, Veterans Administration Medical Center and University of Iowa, Iowa City, Iowa 52246, USA.

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Published January 15, 1998 - More info

Published in Volume 101, Issue 2 on January 15, 1998
J Clin Invest. 1998;101(2):455–463. https://doi.org/10.1172/JCI949.
© 1998 The American Society for Clinical Investigation
Published January 15, 1998 - Version history
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Abstract

Bacterial LPS is a pluripotent agonist for PMNs. Although it does not activate the NADPH-dependent oxidase directly, LPS renders PMNs more responsive to other stimuli, a phenomenon known as "priming." Since the mechanism of LPS-dependent priming is incompletely understood, we investigated its effects on assembly and activation of the NADPH oxidase. LPS pretreatment increased superoxide (O2-) generation nearly 10-fold in response to N-formyl methionyl leucyl phenylalanine (fMLP). In a broken-cell O2--generating system, activity was increased in plasma membrane-rich fractions and concomitantly decreased in specific granule-rich fractions from LPS-treated cells. Oxidation-reduction spectroscopy and flow cytometry indicated LPS increased plasma membrane association of flavocytochrome b558. Immunoblots of plasma membrane vesicles from LPS-treated PMNs demonstrated translocation of p47-phox but not of p67-phox or Rac2. However, PMNs treated sequentially with LPS and fMLP showed a three- to sixfold increase (compared with either agent alone) in plasma membrane-associated p47-phox, p67-phox, and Rac2, and translocation paralleled augmented O2- generation by intact PMNs. LPS treatment caused limited phosphorylation of p47-phox, and plasma membrane-enriched fractions from LPS- and/or fMLP-treated cells contained fewer acidic species of p47-phox than did those from cells treated with PMA. Taken together, these studies suggest that redistribution of NADPH oxidase components may underlie LPS priming of the respiratory burst.

Version history
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