Source:http://linkedlifedata.com/resource/pubmed/id/20190143
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
7
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| pubmed:dateCreated |
2010-3-22
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| pubmed:abstractText |
Macrophages provide a first line of defense against Mycobacterium tuberculosis. However, in instances where macrophage activation for killing is suboptimal, M. tuberculosis is capable of surviving intracellularly. IL-32 is a recently described cytokine induced by M. tuberculosis in a variety of cell types including human monocytes and macrophages. In this study, we investigated the biological significance of IL-32 in an in vitro model of M. tuberculosis infection in differentiated THP-1 human macrophages in which IL-32 expression was silenced using stable expression of short hairpin RNA (shRNA). Inhibition of endogenous IL-32 production in THP-1 cells that express one of three distinct shRNA-IL-32 constructs significantly decreased M. tuberculosis induction of TNF-alpha by approximately 60%, IL-1beta by 30-60%, and IL-8 by 40-50% and concomitantly increased the number of cell-associated M. tuberculosis bacteria compared with THP-1 cells stably expressing a scrambled shRNA. In THP-1 cells infected with M. tuberculosis and stimulated with rIL-32, a greater level of apoptosis was observed compared with that with M. tuberculosis infection alone. Obversely, there was significant abrogation of apoptosis induced by M. tuberculosis and a concomitant decrease in caspase-3 activation in cells depleted of endogenous IL-32. rIL-32gamma significantly reduced the number of viable intracellular M. tuberculosis bacteria, which was modestly but significantly abrogated with a caspase-3 inhibitor. We conclude that IL-32 plays a host defense role against M. tuberculosis in differentiated THP-1 human macrophages.
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| pubmed:grant | |
| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
AIM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:month |
Apr
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| pubmed:issn |
1550-6606
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| pubmed:author | |
| pubmed:issnType |
Electronic
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| pubmed:day |
1
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| pubmed:volume |
184
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
3830-40
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| pubmed:meshHeading |
pubmed-meshheading:20190143-Apoptosis,
pubmed-meshheading:20190143-Blotting, Western,
pubmed-meshheading:20190143-Cell Differentiation,
pubmed-meshheading:20190143-Cell Line,
pubmed-meshheading:20190143-Cytokines,
pubmed-meshheading:20190143-Gene Expression,
pubmed-meshheading:20190143-Humans,
pubmed-meshheading:20190143-In Situ Nick-End Labeling,
pubmed-meshheading:20190143-Interleukins,
pubmed-meshheading:20190143-Macrophages,
pubmed-meshheading:20190143-Mycobacterium tuberculosis,
pubmed-meshheading:20190143-RNA, Small Interfering,
pubmed-meshheading:20190143-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:20190143-Tuberculosis
|
| pubmed:year |
2010
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| pubmed:articleTitle |
IL-32 is a host protective cytokine against Mycobacterium tuberculosis in differentiated THP-1 human macrophages.
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| pubmed:affiliation |
Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado Denver at Anschutz Medical Center, Denver, CO 80045, USA.
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| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, Non-P.H.S.,
Research Support, N.I.H., Extramural
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