Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2008-6-11
pubmed:abstractText
Mycobacterium avium infects mononuclear phagocytes, which thereby become reservoirs for this pathogen. Currently recommended therapy does not ensure the eradication of intracellular bacteria. Here, we report that M. avium infection in macrophages activates the signal transducer and activator of transcription type 1 (STAT-1) signaling pathway. Fludarabine, an antileukemic drug active against cells that express STAT-1, selectively kills M. avium-infected macrophages. These findings suggest that phosphorylated STAT-1 can enhance the survival of macrophages, promoting their role as persistent reservoirs of M. avium. This work invites research on new combination therapeutic approaches that consist of fludarabine, to kill the macrophage reservoir, and antibacterial agents, to eliminate mycobacteria released from the dead cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0022-1899
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
198
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
95-100
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Selective killing of Mycobacterium avium-infected macrophages by inhibition of phosphorylated signal transducer and activator of transcription type 1.
pubmed:affiliation
Institutes of Biochemistry "G. Fornaini", University of Urbino "Carlo Bo," Urbino, Italy.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't