text: PT has been shown to affect the innate immune response. It inhibits the early recruitment of neutrophils and macrophages, and interferes with early chemokine production and neutrophil chemotaxis. Chemokines are signalling molecules produced by infected cells and attract neutrophils and macrophages. Neutrophil chemotaxis is thought to be disrupted by inhibiting G-protein-coupled chemokine receptors by the ADP-ribosylation of G proteins.
  Because of the disrupted signalling pathways, synthesis of chemokines will be affected. This will prevent the infected cell from producing them and thereby inhibiting recruitment of neutrophils. Under normal circumstances, alveolar macrophages and other lung cells produce a variety of chemokines. PT has been found to  inhibit the early transcription of  keratinocyte-derived chemokine, macrophage inflammatory protein 2 and LPS-induced CXC chemokine. Eventually, PT causes lymphocytosis, one of the systemic manifestations of whooping cough.
  PT, a decisive virulence determinant of B. pertussis,  is able to cross the blood–brain barrier by increasing its permeability. 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.