Editors' ChoiceNeuroscience

A little stress is good

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Science Signaling  30 May 2017:
Vol. 10, Issue 481, eaan8358
DOI: 10.1126/scisignal.aan8358

Acute psychological stress triggers signaling between sympathetic neurons and the spleen to protect against ischemic tissue damage.

Inflammation caused by ischemia-reperfusion injury (IRI), which occurs upon tissue reoxygenation after hypoxic trauma—such as stroke, cardiac arrest, sleep apnea, or organ transplant—delays recovery, contributes to fibrosis, and underlies mortality in various conditions. In response to IRI, vagal neurons activate a cholinergic anti-inflammatory pathway (CAP) to limit the duration and extent of inflammation. The sympathetic nervous system, which also responds to psychological stress, might also contribute to anti-inflammatory reflexes. Abe et al. found that acute psychological stress protected against IRI through a sympathetic neuron–activated CAP. Brief physical restraint, which causes psychological stress in mice, activated cholinergic signaling from sympathetic C1 neurons that stimulated immune cell production in the spleen and decreased markers of kidney damage after renal IRI compared with unstressed mice. Similarly, mice were protected from IRI upon optogenetic activation of C1 neurons, injection with splenic immune cells that had been cultured with noradrenaline, or injection with splenocytes harvested from stressed mice. In contrast, restraint stress-induced protection was prevented by inhibiting cholinergic signaling, C1 activity, or splenocyte production. The findings suggest that brief bouts of psychological stress may prime the body against subsequent physical injury through this CNS-to-splenic anti-inflammatory axis. Therapeutically activating this pathway might limit inflammation associated with various diseases, injuries, and organ transplantation.

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