DAT, deacylating autotransporter toxin, from <i>Bordetella parapertussis</i> demyristoylates Gα_i GTPases and contributes to cough.

Abstract

The pathogenic bacteria <i>Bordetella pertussis</i> and <i>Bordetella parapertussis</i> cause pertussis (whooping cough) and pertussis-like disease, respectively, both of which are characterized by paroxysmal coughing. We previously reported that pertussis toxin (PTx), which inactivates heterotrimeric GTPases of the G_i family through ADP-ribosylation of their α subunits, causes coughing in combination with Vag8 and lipid A in <i>B. pertussis</i> infection. In contrast, the mechanism of cough induced by <i>B. parapertussis</i>, which produces Vag8 and lipopolysaccharide (LPS) containing lipid A, but not PTx, remained to be elucidated. Here, we show that a toxin we named deacylating autotransporter toxin (DAT) of <i>B. parapertussis</i> inactivates heterotrimeric G_i GTPases through demyristoylation of their α subunits and contributes to cough production along with Vag8 and LPS. These results indicate that DAT plays a role in <i>B. parapertussis</i> infection in place of PTx.