Using a murine Cecal ligation and puncture (CLP) model of sepsis, the authors show that sepsis leads to reduced activity of orexinergic neurons and that restoring this activity (via an M1 muscarinic acetylcholine receptor agonist or chemogenetic activation of orexin neurons) partially reverses abnormal cytokine responses and splenic innate immune cell changes.
Activation of orexinergic neurons or M1 agonist treatment reversed CLP‑induced increases in TNF‑α and IL‑1β, corrected splenic macrophage and monocyte‑derived dendritic cell numbers; however some cytokines (e.g., IL‑6, KC, G‑CSF) and T cell reductions were unaffected.
Transgenic mouse with orexinergic neurons expressing a DREADD (Designer Receptor Exclusively Activated by a Designer Drug) to enable chemogenetic activation — murine C57BL/6 background
Sepsis, neuro‑immune regulation, orexinergic signaling, cholinergic receptor modulation, immune dysfunction
CLP sepsis model, transgenic DREADD knock‑in in orexin neurons, CNO administration, measurement of vital signs/hormones, cytokine profiling, immune cell phenotyping (splenic macrophages, DCs, T cells)
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