The symptoms of infection are often caused by an exaggerated inflammatory response that engages nerve cells at the site of infection. This is exemplified by acute cystitis, characterized by pain at micturition, dysuria and frequency of urination.
We have shown how nerve cells are activated during acute cystitis and have identified a mechanism of direct bacterial activation of the classic pain agonist Substance P and its receptor. We have also identified the nerve cell response as a component of innate immunity, regulated and closely linked to the inflammasome.
Inhibiting these effects with an NK1R antagonists is an effective approach in animal models. It may also be possible to use a nerve cell transmitter substance as a biomarker, to identify patients suitable for this type of therapy, suggesting a combined diagnostic and therapeutic approach in this patient group.
