Listeria monocytogenes infection induces prosurvival metabolic signaling in macrophages
UMass Chan Affiliations
Department of Molecular Genetics and MicrobiologyProgram in Gene Function and Expression
Document Type
Journal ArticlePublication Date
2011-04-01Keywords
AnimalsApoptosis Regulatory Proteins
Blotting, Western
Female
Gene Expression
Gene Expression Regulation
In Situ Nick-End Labeling
Listeria monocytogenes
Listeriosis
Macrophages
Mice
Mice, Inbred C57BL
Receptors, Immunologic
Reverse Transcriptase Polymerase Chain Reaction
Signal Transduction
Steroid Hydroxylases
Up-Regulation
Genetics and Genomics
Metadata
Show full item recordAbstract
Host cells use metabolic signaling through the LXRalpha nuclear receptor to defend against Listeria monocytogenes infection. 25-Hydroxycholesterol is a natural ligand of LXRs that is produced by the enzyme cholesterol 25-hydroxylase (CH25H). We found that expression of Ch25h is upregulated following L. monocytogenes infection in a beta interferon (IFN-beta)-dependent fashion. Moreover, increased Ch25h expression promotes survival of L. monocytogenes-infected cells and increases sensitivity of the host to infection. We determined that expression of Cd5l, a prosurvival gene, is controlled by CH25H. In addition, we found that CD5L inhibits activation of caspase-1, promoting survival of infected macrophages. Our results reveal a mechanism by which an intracellular pathogen can prolong survival of infected cells, thus providing itself with a protected environment in which to replicate.Source
Infect Immun. 2011 Apr;79(4):1526-35. Epub 2011 Jan 24. Link to article on publisher's siteDOI
10.1128/IAI.01195-10Permanent Link to this Item
http://hdl.handle.net/20.500.14038/43946PubMed ID
21263022Related Resources
Link to Article in PubMedae974a485f413a2113503eed53cd6c53
10.1128/IAI.01195-10