Journal
NATURE NEUROSCIENCE
Volume 20, Issue 11, Pages 1549-+Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nn.4643
Keywords
-
Categories
Funding
- German Academic Exchange Service (DAAD) [D/10/43923]
- German Research Foundation (DFG) [PR 1274/2-1, STU 528/1-1, CRC-914]
- German Research Foundation (Cluster of Excellence NeuroCure)
- Wings for Life Spinal Cord Research Foundation [WfL-DE-006/12]
- Else Kroner Fresenius Stiftung
- German legal accident insurance (DGUV)
- Era-Net-NEURON Program of the European Union
- NIDILRR [90SI5020]
- Ohio State University Discovery Theme
- W.E. Hunt & C.M. Curtis Endowment
- National Institute on Disability, Independent Living, and Rehabilitation Research (NIDILRR) [90DP0083]
- US Department of Health and Human Services
- HMS Center for Immune Imaging
- NIH [AI112521, AR068383]
- NIDILRR [911874, 90SI5020] Funding Source: Federal RePORTER
Ask authors/readers for more resources
Acute spinal cord injury (SCI) causes systemic immunosuppression and life-threatening infections, thought to result from noradrenergic overactivation and excess glucocorticoid release via hypothalamus-pituitary-adrenal axis stimulation. Instead of consecutive hypothalamus-pituitary-adrenal axis activation, we report that acute SCI in mice induced suppression of serum norepinephrine and concomitant increase in cortisol, despite suppressed adrenocorticotropic hormone, indicating primary (adrenal) hypercortisolism. This neurogenic effect was more pronounced after high-thoracic level (Th1) SCI disconnecting adrenal gland innervation, compared with low-thoracic level (Th9) SCI. Prophylactic adrenalectomy completely prevented SCI-induced glucocorticoid excess and lymphocyte depletion but did not prevent pneumonia. When adrenalectomized mice were transplanted with denervated adrenal glands to restore physiologic glucocorticoid levels, the animals were completely protected from pneumonia. These findings identify a maladaptive sympathetic-neuroendocrine adrenal reflex mediating immunosuppression after SCI, implying that therapeutic normalization of the glucocorticoid and catecholamine imbalance in SCI patients could be a strategy to prevent detrimental infections.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available