Increased intracranial pressure induces a rapid systemic interleukin-10 release through activation of the sympathetic nervous system.

There is a bi-directional communication between the immune and central nervous system. In this context, it is known that patients with traumatic brain injury suffered from systemic immunodepression and an increased risk to develop infectious complications. We investigated the role of an increased intracranial pressure (ICP) and sympathetic activation on systemic immune changes. A sustained increase in ICP was achieved by inflation of a subdural balloon. At different time points, plasma levels of the anti-inflammatory cytokine, interleukin (IL)-10, were measured. Furthermore, the effect of a sympathetic blockade by co-administration of the beta2-adreoreceptor antagonist, propranolol, was evaluated. Finally, we examined the impact of epinephrine infusion on blood IL-10 levels. We showed that an increase in ICP with activation of the sympathetic nervous system was able to induce systemic release of IL-10. This effect was blocked by administration of the beta2-adreoreceptor antagonist. Furthermore, epinephrine infusion directly induced systemic release of IL-10. Our data suggested that sympathetic activation with release of epinephrine may induce systemic immunodepression with risk of infectious complications in brain-injured patients.