Reduced glial activity after surgery: A sign of immunoparalysis of the brain?
With respect to neurological conditions, we previously demonstrated that increased vagal activity is associated with inhibition of systemic innate immune parameters, including reduced immunoreactivity of peripheral blood cells, in critically ill patients with brain damage.4 As vagal activity is increased in traumatic brain injury, a vagally induced immunoparalytic state could contribute to the high prevalence of infections in these patients.
The study of Forsberg et al adds to the growing literature that links innate immune responses to neurological diseases. Previous animal work and studies in healthy individuals have shown that acute systemic inflammation induces a neuroinflammatory response as well.5 The latter has also been associated with cognitive impairment and subsequent neurodegenerative diseases. However, this recent article1 is the first to indicate that immunoparalysis is not only a systemic phenomenon, but also may be present in the brain. This is still largely uncharted territory. One may argue that this may represent an endogenous protective mechanism to prevent immunopathology to the brain. If so, reversing immunoparalysis by boosting the innate immune response in the acute phase postsurgery may be detrimental for the brain.
Although the brain was long viewed as an immune privileged organ, it is now clear that we need more studies to understand the critical role the innate immune system could play in neurological diseases.