[3] Research suggests PT may have a therapeutic role in treating a number of common human ailments, including hypertension,[4] viral infection,[5] and autoimmunity.

Another epidemic of pertussis took place in Paris in 1578 and was described by a contemporary observer, Guillaume de Baillou.

Jules Bordet and Octave Gengou described in 1900 the finding of a new “ovoid bacillus” in the sputum of a 6-month-old infant with whooping cough.

Bordetella parapertussis shows the most similarity to B. pertussis and was therefore used for research determining the role of PT in causing the typical symptoms of whooping cough.

Rats infected with B. parapertussis or a PT-deficient mutant of B. pertussis did not show this symptom; neither of these two strains produced PT.

Following PT binding to a cell membrane receptor, it is taken up in an endosome, after which it undergoes retrograde transport to the trans-Golgi network and endoplasmic reticulum.

This prevents the G proteins from interacting with G protein-coupled receptors on the cell membrane, thus interfering with intracellular communication.

[17] The Gi subunits remain locked in their GDP-bound, inactive state, thus unable to inhibit adenylate cyclase activity, leading to increased cellular concentrations of cAMP.

[18] As a result of this unique mechanism, PT has also become widely used as a biochemical tool to ADP-ribosylate GTP-binding proteins in the study of signal transduction.

Neutrophil chemotaxis is thought to be disrupted by inhibiting G-protein-coupled chemokine receptors by the ADP-ribosylation of Gi proteins.

[22] As a result, PT can cause severe neurological complications; however, recently it has been found that the medicinal usage of Pertussis toxin can promote the development of regulatory T cells and prevent central nervous system autoimmune disease, such as multiple sclerosis.

Countries with a documented spread of ptxP3 include Australia,[26][27] Denmark,[28] Finland,[29] Iran,[30] Italy,[31] Japan,[32] the Netherlands,[33] and Sweden.