| The UPEC Pore-Forming Toxin α-Hemolysin Triggers Proteolysis of Host Proteins to Disrupt Cell Adhesion, Inflammatory, and Survival Pathways. | |
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MedLine Citation:
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PMID: 22264513 Owner: NLM Status: In-Data-Review |
Abstract/OtherAbstract:
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Uropathogenic Escherichia coli (UPEC), which are the leading cause of both acute and chronic urinary tract infections, often secrete a labile pore-forming toxin known as α-hemolysin (HlyA). We show that stable insertion of HlyA into epithelial cell and macrophage membranes triggers degradation of the cytoskeletal scaffolding protein paxillin and other host regulatory proteins, as well as components of the proinflammatory NFκB signaling cascade. Proteolysis of these factors requires host serine proteases, and paxillin degradation specifically involves the serine protease mesotrypsin. The induced activation of mesotrypsin by HlyA is preceded by redistribution of mesotrypsin precursors from the cytosol into foci along microtubules and within nuclei. HlyA intoxication also stimulated caspase activation, which occurred independently of effects on host serine proteases. HlyA-induced proteolysis of host proteins likely allows UPEC to not only modulate epithelial cell functions, but also disable macrophages and suppress inflammatory responses. |
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Authors:
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Bijaya K Dhakal; Matthew A Mulvey |
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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: 58-69 Citation Subset: IM |
Copyright Information:
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Copyright © 2012 Elsevier Inc. All rights reserved. |
Affiliation:
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Division of Microbiology and Immunology, Pathology Department, University of Utah School of Medicine, Salt Lake City, Utah, USA 84112-0565. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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