Abstract:
:Bacillus anthracis, the etiologic agent of anthrax, avoids immune surveillance and commandeers host macrophages as a vehicle for lymphatic spreading. Here, we show that B. anthracis edema toxin (ET), via its adenylyl cyclase activity, dramatically increases the motility of infected macrophages and the expression of vascular endothelial growth factor. The transcription factor CREB and the syndecan-1 gene, a CREB target, play crucial roles in ET-induced macrophage migration. These molecular and cellular responses occur in macrophages engaged in antiinflammatory G protein-coupled receptor activation, thus illustrating a common signaling circuitry controlling resolution of inflammation and host cell hijacking by B. anthracis.
journal_name
Proc Natl Acad Sci U S Aauthors
Kim C,Wilcox-Adelman S,Sano Y,Tang WJ,Collier RJ,Park JMdoi
10.1073/pnas.0800105105subject
Has Abstractpub_date
2008-04-22 00:00:00pages
6150-5issue
16eissn
0027-8424issn
1091-6490pii
0800105105journal_volume
105pub_type
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