Serratia marcescens Induces Apoptotic Cell Death in Host Immune Cells via a Lipopolysaccharide- and Flagella-dependent Mechanism

Injection of Serratia marcescens into the blood (hemolymph) of the silkworm, Bombyx mori, induced the activation of c-Jun NH2-terminal kinase (JNK), followed by caspase activation and apoptosis of blood cells (hemocytes). This process impaired the innate immune response in which pathogen cell wall c...

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Bibliographic Details
Published in:The Journal of biological chemistry 2012-10, Vol.287 (43), p.36582-36592
Main Authors: Ishii, Kenichi, Adachi, Tatsuo, Imamura, Katsutoshi, Takano, Shinya, Usui, Kimihito, Suzuki, Kazushi, Hamamoto, Hiroshi, Watanabe, Takeshi, Sekimizu, Kazuhisa
Format: Article
Language:English
Subjects:
Animals
Apoptosis
Apoptosis - immunology
Bacterial Proteins - immunology
Bombyx - immunology
Bombyx - microbiology
Flagella - immunology
Hemocytes - immunology
Hemocytes - microbiology
Immunity, Innate
Innate Immunity
Insect Immunity
Lipopolysaccharide (LPS)
Lipopolysaccharides - immunology
Macrophages
Macrophages, Peritoneal - immunology
Macrophages, Peritoneal - microbiology
Membrane Proteins - immunology
Mice
Microbiology
Serratia Infections - immunology
Serratia Infections - microbiology
Serratia marcescens - immunology
Serratia marcescens - metabolism
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Summary:Injection of Serratia marcescens into the blood (hemolymph) of the silkworm, Bombyx mori, induced the activation of c-Jun NH2-terminal kinase (JNK), followed by caspase activation and apoptosis of blood cells (hemocytes). This process impaired the innate immune response in which pathogen cell wall components, such as glucan, stimulate hemocytes, leading to the activation of insect cytokine paralytic peptide. S. marcescens induced apoptotic cell death of silkworm hemocytes and mouse peritoneal macrophages in vitro. We searched for S. marcescens transposon mutants with attenuated ability to induce apoptosis of silkworm hemocytes. Among the genes identified, disruption mutants of wecA (a gene involved in lipopolysaccharide O-antigen synthesis), and flhD and fliR (essential genes in flagella synthesis) showed reduced motility and impaired induction of mouse macrophage cell death. These findings suggest that S. marcescens induces apoptosis of host immune cells via lipopolysaccharide- and flagella-dependent motility, leading to the suppression of host innate immunity. Background: The pathogenic mechanism of Serratia marcescens is poorly understood. Results:S. marcescens kills immune cells via an lipopolysaccharide- and flagella-dependent mechanism. Conclusion:S. marcescens suppresses innate immunity by killing immune cells. Significance: This is the first evidence to suggest that S. marcescens evades the immune system.
ISSN:0021-9258
1083-351X
DOI:10.1074/jbc.M112.399667