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Reduced glial activity after surgery: A sign of immunoparalysis of the brain?

With great interest we read the article by Forsberg et al on the immune response of the human brain following abdominal surgery, representing the first in vivo imaging study of surgeryinduced neuroinflammation. Forsberg and colleagues demonstrated profound downregulation of the brain glial activity in the early postoperative period. This surprising result coincided with a reduction in immunoreactivity of peripheral blood cells, a well-known hallmark of an immunosuppressed state known as “immunoparalysis.” We and others have shown that this immunoparalysis occurs in patients with sepsis and trauma and likely contributes to the high mortality in critically ill patients. Indeed, critically ill patients who survive the initial cytokine response following sepsis, surgery, or trauma may often suffer from severe and sometimes lethal secondary infections due to this immunosuppressed state. The progress in understanding the role of innate immune responses in critical illnesses has resulted in a paradigm shift, whereby the focus for novel therapies went from inhibiting the initial to stimulating the overriding immune response. 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. 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. The latter has also been associated with cognitive impairment and subsequent neurodegenerative diseases. However, this recent article 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.