Abstract
Listeria monocytogenes (Lm), a facultative anaerobic gram-positive bacterium, causes listeriosis. Immune cell apoptosis is considered to be one pathogenic factor for listeriosis. As a deubiquitinase, CYLD is an important regulator both in innate immune response and apoptosis by negatively modulating NF-κB pathway. However the role of CYLD in Lm induced apoptosis remains unclear. Here we found that CYLD is significantly up-regulated in macrophages upon its infection. There is a moderate decrease in Lm proliferation and apoptotic cells in siRNA-induced CYLD knockdown THP-1 cells. Thereby CYLD may be involved in cell apoptosis mediated by Lm infection and its proliferation.
Keywords:
Apoptosis; CYLD; Listeria monocytogenes.
Copyright © 2015 Elsevier Ltd. All rights reserved.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Apoptosis / immunology
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Cell Line
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Deubiquitinating Enzyme CYLD
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Flow Cytometry
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Gene Knockdown Techniques
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Humans
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Immunity, Innate
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Listeria monocytogenes / immunology*
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Listeria monocytogenes / metabolism*
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Listeria monocytogenes / pathogenicity
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Listeriosis / immunology*
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Listeriosis / metabolism
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Listeriosis / microbiology
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Macrophages / immunology*
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Macrophages / metabolism
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Macrophages / microbiology*
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NF-kappa B / immunology
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NF-kappa B / metabolism
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RNA, Small Interfering / administration & dosage
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RNA, Small Interfering / genetics
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Transcriptional Activation
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Tumor Suppressor Proteins / genetics
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Tumor Suppressor Proteins / immunology*
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Tumor Suppressor Proteins / metabolism
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Up-Regulation / immunology
Substances
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NF-kappa B
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RNA, Small Interfering
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Tumor Suppressor Proteins
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CYLD protein, human
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Deubiquitinating Enzyme CYLD