Anthracis edema toxin is a toxin that increases cAMP levels.
Anthrax edema toxin, produced by Bacillus anthracis, elevates intracellular cyclic AMP (cAMP) concentrations in host cells. This increase in cAMP is a key mechanism by which the toxin disrupts cellular function and contributes to the pathogenesis of anthrax. Specifically, the edema factor (EF) component of the toxin is an adenylate cyclase. Adenylate cyclase is an enzyme that catalyzes the conversion of ATP to cAMP. When EF enters host cells, it uses cellular ATP to produce supraphysiological levels of cAMP.
The elevated cAMP levels then disrupt various cellular signaling pathways and functions. For example, increased cAMP can activate protein kinase A (PKA), which phosphorylates a wide range of target proteins, leading to altered cellular activity. This dysregulation of signaling pathways contributes to edema (swelling), impaired immune cell function, and other manifestations of anthrax. The study mentioned in the references indicates that this process can inhibit phenylephrine-stimulated contraction in a rat aortic ring model, demonstrating the toxin's effect on vascular function through the cAMP pathway.
Therefore, Bacillus anthracis edema toxin, through its edema factor component, directly increases cAMP concentrations within host cells.
