Open AccessAnthrax Edema Toxin Inhibits Nox1-Mediated Formation of Reactive Oxygen Species by Colon Epithelial Cells
Author(s) -
Jun-Sub Kim,
Gary M. Bokoch
Publication year - 2008
Publication title -
journal of innate immunity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.078
H-Index - 64
eISSN - 1662-8128
pISSN - 1662-811X
DOI - 10.1159/000151481
Subject(s) - nox1 , bacillus anthracis , innate immune system , anthrax toxin , microbiology and biotechnology , reactive oxygen species , biology , nadph oxidase , immune system , chemistry , immunology , biochemistry , bacteria , recombinant dna , genetics , gene , fusion protein
One major route of intoxication by Bacillus anthracis (anthrax) spores is via their ingestion and subsequent uptake by the intestinal epithelium. Anthrax edema toxin (ETx) is an adenylate cyclase that causes persistent elevation of cAMP in intoxicated cells. NADPH oxidase enzymes (Nox1-Nox5, Duox1 and 2) generate reactive oxygen species (ROS) as components of the host innate immune response to bacteria, including Nox1 in gastrointestinal epithelial tissues. We show that ETx effectively inhibits ROS formation by Nox1 in HT-29 colon epithelial cells. This inhibition requires the PKA-mediated phosphorylation of the Nox1-regulatory component, NoxA1, and the subsequent binding of 14-3-3zeta. Inhibition of Nox1-mediated ROS formation in the gut epithelium may be a mechanism used by B. anthracis to circumvent the innate immune response.