Anthrax Research Today is a free monthly online journal that collates and summarizes the latest research about Anthrax, including details on bacillus anthracis, contagiousness, exposure, effects.

Antiinflammatory cAMP signaling and cell migration genes co-opted by the anthrax bacillus.

Kim C, Wilcox-Adelman S, Sano Y, Tang WJ, Collier RJ, Park JM

Cutaneous Biology Research Center, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA 02129, USA.

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.

Published 23 April 2008 in Proc Natl Acad Sci U S A, 105(16): 6150-5.
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