The hemolytic and cytolytic activities of <it>Serratia marcescens </it>phospholipase A (PhlA) depend on lysophospholipid production by PhlA

<p>Abstract</p> <p>Background</p> <p><it>Serratia marcescens </it>is a gram-negative bacterium and often causes nosocomial infections. There have been few studies of the virulence factors of this bacterium. The only <it>S. marcescens </it>hemolyt...

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Bibliographic Details
Main Authors: Koizumi Nobuo, Gotoh Naomasa, Iyoda Sunao, Ohnishi Makoto, Shimuta Ken, Watanabe Haruo
Format: Article
Language:English
Published: BMC 2009-12-01
Series:BMC Microbiology
Online Access:http://www.biomedcentral.com/1471-2180/9/261
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Summary:<p>Abstract</p> <p>Background</p> <p><it>Serratia marcescens </it>is a gram-negative bacterium and often causes nosocomial infections. There have been few studies of the virulence factors of this bacterium. The only <it>S. marcescens </it>hemolytic and cytotoxic factor reported, thus far, is the hemolysin ShlA.</p> <p>Results</p> <p>An <it>S. marcescens shl</it>AB deletion mutant was constructed and shown to have no contact hemolytic activity. However, the deletion mutant retained hemolytic activity on human blood agar plates, indicating the presence of another <it>S. marcescens </it>hemolytic factor. Functional cloning of <it>S. marcescens </it>identified a phospholipase A (PhlA) with hemolytic activity on human blood agar plates. A <it>phl</it>AB deletion mutant lost hemolytic activity on human blood agar plates. Purified recombinant PhlA hydrolyzed several types of phospholipids and exhibited phospholipase A1 (PLA1), but not phospholipase A2 (PLA2), activity. The cytotoxic and hemolytic activities of PhlA both required phospholipids as substrates.</p> <p>Conclusion</p> <p>We have shown that the <it>S. marcescens phlA </it>gene produces hemolysis on human blood agar plates. PhlA induces destabilization of target cell membranes in the presence of phospholipids. Our results indicated that the lysophospholipids produced by PhlA affected cell membranes resulting in hemolysis and cell death.</p>
ISSN:1471-2180