Evaluation of innate lymphoid cells and long-term cognition in a rat model of experimental sepsis

Abstract

Abstract Background Sepsis is characterized as a critical condition involving life-threatening organ dysfunction stemming from an imbalanced host immune response to infections. Survivors of sepsis face an increased risk of post-hospital discharge mortality along with potential long-term cognitive and functional impairments. Recent research has uncovered the roles of innate lymphoid cells (ILCs) in the borders of the central nervous system (CNS), extending beyond their well-established functions in immune regulation and neuroinflammation. ILCs may play a pivotal role in the pathophysiology of sepsis, influencing immunity, inflammation, and brain barrier homeostasis. Here we investigated the role of subtypes ILC1, ILC2, and ILC3 on experimental sepsis-induced cognitive decline. Methods Adult male Wistar rats were submitted to sepsis by cecal ligation and perforation (CLP) surgery or sham (non-CLP) surgery as the control group. Ten days after sepsis induction, all the rats were submitted to a novel object recognition (NOR) task, a non-spatial, declarative memory known as recognition memory and were euthanized. The presence of ILCs was evaluated in the choroid plexus (CP), meninges, brain, spleen, and gut using multi-channel flow cytometry. Results We observed that Wistar rats recovered from sepsis showed deficits in recognition memory, with no discernible difference in the count of ILCs between the CLP and non-CLP groups. However, we found a significant difference between ILC subtypes in the meninges and CP in the CLP group. Conclusions This finding further reinforces the notion that sepsis survivors commonly experience cognitive deficits post-recovery. Additionally, it implies that the involvement of specific ILCs subtypes may be significant during the acute phase of sepsis pathophysiology, but their impact diminishes after the recovery period.