The S-nitrosylation of Peroxiredoxin 1 during Bacillus anthracis Infection in Human Small Airway Epithelial Cells
Date
2012-10-09
Authors
Hamer, Sarah G.
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Abstract
Bacillus anthracis, a Gram-positive soil bacterium, is the causative agent of anthrax. B. anthracis is classified as a “Category A” agent by the Centers for Disease Control and Prevention. Although the key virulence factors of anthrax are the toxins (i.e. lethal toxin and edema toxin), it has been proven that the bacterial nitric oxide synthase (bNOS) of B. anthracis also plays a role in pathogenesis. Since B. anthracis infection produces nitric oxide that is responsible for S-nitrosylation of host proteins, it was hypothesized that bNOS-induced nitric oxide contributes to the regulation of functions in host cells through modifications of proteins. Nitrosoproteomic analysis using the biotin switch technique demonstrated that during B. anthracis infection, S-nitrosylation of peroxiredoxin 1 (Prx1) in human small airway epithelial cells (HASECs) was increased. When Prx1 was S-nitrosylated, there was a decrease in its peroxidase activity and an increase in its chaperone activity. Treatment with a nitric oxide donor to ensure that proteins were S-nitrosylated showed that in an environment that contained hydrogen peroxide, S-nitrosylation contributed to a decrease in cell viability. However, during early B. anthracis infection, S-nitrosylation of HSAECs proteins increased cell viability, presumably due to Prx1 increased chaperone activity when S-nitrosylated. It can be concluded that during the early stages of B. anthracis infection, nitric oxide produced by B. anthracis causes the S-nitrosylation of Prx1, which may contribute to an early-stage protection (an increase in viability) of HSAECs.
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Keywords
S-nitrosylation, Peroxiredoxin 1, Human small airway epithelial cells, Bacillus anthracis