C1 neurons mediate a stress-induced anti-inflammatory reflex in mice.

Chikara Abe, Tsuyoshi Inoue, Mabel A Inglis, Kenneth E Viar, Liping Huang, Hong Ye, Diane L Rosin, Ruth L Stornetta, Mark D Okusa, Patrice G Guyenet

Nature neuroscience 2017 May

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C1 neurons, located in the medulla oblongata, mediate adaptive autonomic responses to physical stressors (for example, hypotension, hemorrhage and presence of lipopolysaccharides). We describe here a powerful anti-inflammatory effect of restraint stress, mediated by C1 neurons: protection against renal ischemia-reperfusion injury. Restraint stress or optogenetic C1 neuron (C1) stimulation (10 min) protected mice from ischemia-reperfusion injury (IRI). The protection was reproduced by injecting splenic T cells that had been preincubated with noradrenaline or splenocytes harvested from stressed mice. Stress-induced IRI protection was absent in Chrna7 knockout (a7nAChR-/-) mice and greatly reduced by destroying or transiently inhibiting C1. The protection conferred by C1 stimulation was eliminated by splenectomy, ganglionic-blocker administration or β2-adrenergic receptor blockade. Although C1 stimulation elevated plasma corticosterone and increased both vagal and sympathetic nerve activity, C1-mediated IRI protection persisted after subdiaphragmatic vagotomy or corticosterone receptor blockade. Overall, acute stress attenuated IRI by activating a cholinergic, predominantly sympathetic, anti-inflammatory pathway. C1s were necessary and sufficient to mediate this effect.

Citation

Chikara Abe, Tsuyoshi Inoue, Mabel A Inglis, Kenneth E Viar, Liping Huang, Hong Ye, Diane L Rosin, Ruth L Stornetta, Mark D Okusa, Patrice G Guyenet. C1 neurons mediate a stress-induced anti-inflammatory reflex in mice. Nature neuroscience. 2017 May;20(5):700-707