| Phospholipid Scramblase 1 Mediates Type I Interferon-Induced Protection against Staphylococcal α-Toxin. | |
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MedLine Citation:
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PMID: 22264514 Owner: NLM Status: In-Data-Review |
Abstract/OtherAbstract:
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The opportunistic gram-positive pathogen Staphylococcus aureus is a leading cause of pneumonia and sepsis. Staphylococcal α-toxin, a prototypical pore-forming toxin, is a major virulence factor of S. aureus clinical isolates, and lung epithelial cells are highly sensitive to α-toxin's cytolytic activity. Type I interferon (IFN) signaling activated in response to S. aureus increases pulmonary cell resistance to α-toxin, but the underlying mechanisms are uncharacterized. We show that IFNα protects human lung epithelial cells from α-toxin-induced intracellular ATP depletion and cell death by reducing extracellular ATP leakage. This effect depends on protein palmitoylation and induction of phospholipid scramblase 1 (PLSCR1). IFNα-induced PLSCR1 associates with the cytoskeleton after exposure to α-toxin, and cellular depletion of PLSCR1 negates IFN-induced protection from α-toxin. PLSCR1-deficient mice display enhanced sensitivity to inhaled α-toxin and an α-toxin-producing S. aureus strain. These results uncover PLSCR1 activity as part of an innate protective mechanism to a bacterial pore-forming toxin. |
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Authors:
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Miroslaw Lizak; Timur O Yarovinsky |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Cell host & microbe Volume: 11 ISSN: 1934-6069 ISO Abbreviation: Cell Host Microbe Publication Date: 2012 Jan |
Date Detail:
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Created Date: 2012-01-23 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 101302316 Medline TA: Cell Host Microbe Country: United States |
Other Details:
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Languages: eng Pagination: 70-80 Citation Subset: IM |
Copyright Information:
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Copyright © 2012 Elsevier Inc. All rights reserved. |
Affiliation:
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Section of Cardiovascular Medicine, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT, USA. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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