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

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.
AuthorsChun Kim, Sarah Wilcox-Adelman, Yasuyo Sano, Wei-Jen Tang, R John Collier, Jin Mo Park
JournalProceedings of the National Academy of Sciences of the United States of America (Proc Natl Acad Sci U S A) Vol. 105 Issue 16 Pg. 6150-5 (Apr 22 2008) ISSN: 1091-6490 [Electronic] United States
PMID18427110 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't)
Chemical References
  • Antigens, Bacterial
  • Bacterial Toxins
  • Creb1 protein, mouse
  • Cyclic AMP Response Element-Binding Protein
  • Receptors, G-Protein-Coupled
  • Sdc1 protein, mouse
  • Syndecan-1
  • Vascular Endothelial Growth Factor A
  • anthrax toxin
  • Cyclic AMP
  • Adenylyl Cyclases
Topics
  • Adenylyl Cyclases (metabolism)
  • Animals
  • Anthrax (genetics, immunology, microbiology)
  • Antigens, Bacterial (metabolism)
  • Bacillus anthracis (enzymology)
  • Bacterial Toxins (metabolism)
  • Cell Movement (genetics)
  • Cyclic AMP (metabolism)
  • Cyclic AMP Response Element-Binding Protein (metabolism)
  • Gene Expression Regulation
  • Inflammation (genetics, immunology, microbiology)
  • Macrophages (immunology, microbiology)
  • Mice
  • Mice, Knockout
  • Receptors, G-Protein-Coupled (genetics)
  • Signal Transduction
  • Syndecan-1 (genetics)
  • Up-Regulation
  • Vascular Endothelial Growth Factor A (genetics)

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