POSTOPERATIVE IL-17–ASSOCIATED IMMUNE RESPONSES CORRELATE WITH HIPPOCAMPAL DYSFUNCTION AND COGNITIVE IMPAIRMENT

Surgery induces a systemic inflammatory response that can be accompanied by prolonged cognitive impairment, yet the immune processes linking perioperative inflammation to hippocampal dysfunction remain unclear. Using a mouse model of surgery, we examined postoperative changes in IL-17–associated immune responses and their relationship to neuroinflammation and cognition.

We observed a biphasic inflammatory profile following surgery, characterized by an early increase in hippocampal interleukin-1β (IL-1β) and a sustained elevation of interleukin-17 (IL-17) at later postoperative stages. These immune changes were accompanied by persistent glial activation and deficits in hippocampus-dependent memory. In parallel, IL-17⁺ immune cell populations were increased in peripheral blood and were detectable in the brain after surgery. Pharmacological inhibition of RORγt, a transcriptional regulator associated with IL-17–related immune differentiation, was associated with improved postoperative cognitive performance.

Ongoing work focuses on further characterizing IL-17⁺ immune cell features and spatial distribution following surgery and examining how IL-1β/IL-1 receptor signalling may influence perioperative immune responses. Together, these findings identify IL-17–associated immune alterations as a consistent feature of postoperative neuroinflammation and suggest that immune profiling may provide insight into mechanisms and potential intervention windows in perioperative neurocognitive disorders.