The pathogenic bacteria
Bordetella pertussis
and
Bordetella parapertussis
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
B. pertussis
infection. In contrast, the mechanism of cough induced by
B. parapertussis
, 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
B. parapertussis
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
B. parapertussis
infection in place of PTx.