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.
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Authors | Chun Kim, Sarah Wilcox-Adelman, Yasuyo Sano, Wei-Jen Tang, R John Collier, Jin Mo Park |
Journal | Proceedings 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 |
PMID | 18427110
(Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't)
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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
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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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