{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,4]],"date-time":"2026-09-04T05:16:33Z","timestamp":1788498993752,"version":"build-2803163510"},"reference-count":68,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,9,4]],"date-time":"2026-09-04T00:00:00Z","timestamp":1788480000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Sepsis-associated encephalopathy (SAE) is a syndrome of cerebral dysfunction secondary to sepsis. Although the \u03b17 nicotinic acetylcholine receptor (\u03b17nAChR) plays a pivotal role in the SAE, the specific mechanisms by which it mediates neuroinflammatory responses and contributes to pathological injury in SAE remain unclear.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      The serum \u03b17nAChR level was measured in all included patients. The ROC curve was used to analyze the \u03b17nAChR level for predicting the risk of SAE. The sepsis rat model was constructed by cecal ligation puncture (CLP). The \u03b17nAChR was activated and inhibited by PNU282987 and Methyllycaconitine (MLA) respectively. Cognitive function and neuronal damage were evaluated using behavioral experiment, Nissl staining, Golgi staining and Electron microscopy. Autophagy was examined by Western blot (WB) and transmission electron microscope (TEM).\n                      <jats:italic>In vitro<\/jats:italic>\n                      experiments, lipopolysaccharide (LPS) was used to construct the model of U118. After knockdown and overexpression of \u03b17nAChR, the autophagy proteins level was detected by western blot and the level of cell supernatant inflammatory factors were detected by ELISA. Intracellular calcium concentration was evaluated by flow cytometry.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      The serum \u03b17nAChR levels in SAE patients were lower than that in the healthy controls and sepsis patients, and the its AUC for predicting the risk of SAE was 0.79 (95% CI, 0.68\u20130.90). Activation of the \u03b17nAChR elevated neurobehavioral scores, increased the number of Nissl bodies and synapses, and improved dendritic spine morphology in rats. Activation of \u03b17nAChR weakened the activation of astrocytes, thereby reducing the release of IL-1\u03b2, IL-6 and TNF-\u03b1. The activation of \u03b17nAChR inhibited the level of P62, up-regulated the expression of LC3.\n                      <jats:italic>In vitro<\/jats:italic>\n                      , \u03b17nAChR promoted LPS-induced autophagy in U118 cells, increased intracellular calcium (Ca\n                      <jats:sup>2+<\/jats:sup>\n                      ) concentrations, elevated p-CAMKK2\/CAMKK2 and p-AMPK\/AMPK levels, and decreases p-mTOR\/mTOR levels.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      \u03b17nAChR can alleviate cognitive dysfunction in SAE by activating the Ca\n                      <jats:sup>2+<\/jats:sup>\n                      \/CaMKK2\/AMPK\/mTOR signaling pathway and promoting autophagy in astrocytes.\n                    <\/jats:p>\n                  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