What enzyme's increased activity results in neutrophil chemotaxis and oxidative metabolism impairment in pertussis patients?

In patients with pertussis, an increase in adenylyl cyclase activity leads to elevated cyclic AMP (cAMP) levels within cells. The pertussis toxin, produced by Bordetella pertussis, modifies G proteins that regulate adenylyl cyclase, resulting in excessive production of cAMP. Elevated cAMP levels have widespread effects on immune cell function, particularly neutrophils.

The increased cAMP impairs neutrophil chemotaxis, which is the process by which neutrophils are directed to sites of infection or inflammation. This impairment is significant because effective chemotaxis is essential for the immune response to pathogens. Furthermore, the altered signaling also affects oxidative metabolism in neutrophils, which is crucial for their ability to kill bacteria through the production of reactive oxygen species.

Thus, the increased activity of adenylyl cyclase, driven by the pertussis toxin, disrupts normal neutrophil function, leading to decreased responsiveness and a compromised immune response during a pertussis infection. This understanding highlights the role of cAMP as a critical mediator in immune cell behavior and its modulation by pathogens.