Evidence map›Paper›PMID 28920935›Full record

ArticleNature neuroscience2017

Spinal cord injury-induced immunodeficiency is mediated by a sympathetic-neuroendocrine adrenal reflex.

Harald Prüss, Andrea Tedeschi, Aude Thiriot, Lydia Lynch, Scott M Loughhead, Susanne Stutte, Irina B Mazo, Marcel A Kopp, Benedikt Brommer, Christian Blex and 10 more

Abstract read
PubMed Publisher
In one paragraph

Article in Nature neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
110citing papers in PubMed, 1 pooled it
8.0field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

110 citing papers in PubMed, 1 synthesis or guideline pooled it, 173 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Transcriptomics Insights into Spinal Cord Injury for Therapy Development.International journal of molecular sciences · 2026
    Review
  5. Article
  6. Article
  7. Peripheral Immune Remodeling After Spinal Cord Injury: Marked by Expansion of CD38Neurology(R) neuroimmunology & neuroinflammation · 2026
    Observational
  8. Article
  9. Review
  10. Observational
  11. Lesion level and severity acutely influence metabolomic profiles in spinal cord injury.Journal of neuropathology and experimental neurology · 2026
    Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Correlating autonomic physiology with symptoms of autonomic dysreflexia after spinal cord injury.PM & R : the journal of injury, function, and rehabilitation · 2025
    Article
  20. Article

50 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

20 authors at 8 institutions in 2 countries.

Harald PrüssDepartment of Microbiology and Immunobiology, Division of Immunology, Harvard Medical School, Boston, Massachusetts, USA.ORCID http://orcid.org/0000-0002-8283-7976
Andrea TedeschiBoston Children's Hospital, F.M. Kirby Neurobiology Center, Center for Life Science, Harvard Medical School, Boston, Massachusetts, USA.
Aude ThiriotDepartment of Microbiology and Immunobiology, Division of Immunology, Harvard Medical School, Boston, Massachusetts, USA.
Lydia LynchDepartment of Microbiology and Immunobiology, Division of Immunology, Harvard Medical School, Boston, Massachusetts, USA.
Scott M LoughheadDepartment of Microbiology and Immunobiology, Division of Immunology, Harvard Medical School, Boston, Massachusetts, USA.
Susanne StutteDepartment of Microbiology and Immunobiology, Division of Immunology, Harvard Medical School, Boston, Massachusetts, USA.ORCID http://orcid.org/0000-0003-0277-6403
Irina B MazoDepartment of Microbiology and Immunobiology, Division of Immunology, Harvard Medical School, Boston, Massachusetts, USA.
Marcel A KoppDepartment of Neurology and Experimental Neurology, Clinical and Experimental Spinal Cord Injury Research (Neuroparaplegiology), Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany.ORCID http://orcid.org/0000-0001-6832-9599
Benedikt BrommerDepartment of Neurology and Experimental Neurology, Clinical and Experimental Spinal Cord Injury Research (Neuroparaplegiology), Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany.ORCID http://orcid.org/0000-0003-3362-9780
Christian BlexDepartment of Neurology and Experimental Neurology, Clinical and Experimental Spinal Cord Injury Research (Neuroparaplegiology), Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany.
Laura-Christin GeurtzDepartment of Neurology and Experimental Neurology, Clinical and Experimental Spinal Cord Injury Research (Neuroparaplegiology), Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany.
Thomas LiebscherTreatment Centre for Spinal Cord Injuries, Trauma Hospital Berlin, Berlin, Germany.ORCID http://orcid.org/0000-0002-6025-6564
Andreas NiedeggenTreatment Centre for Spinal Cord Injuries, Trauma Hospital Berlin, Berlin, Germany.
Ulrich DirnaglDepartment of Neurology and Experimental Neurology, Clinical and Experimental Spinal Cord Injury Research (Neuroparaplegiology), Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany.ORCID http://orcid.org/0000-0003-0755-6119
Frank BradkeGerman Center for Neurodegenerative Diseases (DZNE), Bonn, Germany.
Magdalena S VolzDepartment of Gastroenterology, Infectiology and Rheumatology, Charité - Universitätsmedizin Berlin, Berlin, Germany.
Michael J DeVivoNational Spinal Cord Injury Statistical Center, Department of Physical Medicine and Rehabilitation, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Yuying ChenNational Spinal Cord Injury Statistical Center, Department of Physical Medicine and Rehabilitation, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Ulrich H von AndrianDepartment of Microbiology and Immunobiology, Division of Immunology, Harvard Medical School, Boston, Massachusetts, USA.ORCID http://orcid.org/0000-0003-4231-2283
Jan M SchwabDepartment of Neurology and Experimental Neurology, Clinical and Experimental Spinal Cord Injury Research (Neuroparaplegiology), Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany.ORCID http://orcid.org/0000-0001-6784-4919
Harvard University · USHumboldt-Universität zu Berlin · DEBoston Children's Hospital · USDiagnostic and Treatment Centre Berlin · DEGerman Center for Neurodegenerative Diseases · DEUniversity of Alabama at Birmingham · USCharité - Universitätsmedizin Berlin · DEThe Ohio State University Wexner Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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.

Indexed as

AdrenalectomyAdrenal GlandsAdultAgedAnimalsFemaleHumansHypothalamo-Hypophyseal SystemImmune ToleranceMaleMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicMiddle AgedPituitary-Adrenal System

Identifiers

PMID28920935
OpenAlexW2755372493

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.