Immune dysfunction after spinal cord injury - A review of autonomic and neuroendocrine mechanisms

Kyleigh A Rodgers; Kristina A Kigerl; Jan M Schwab; Phillip G Popovich

doi:10.1016/j.coph.2022.102230

Immune dysfunction after spinal cord injury - A review of autonomic and neuroendocrine mechanisms

Curr Opin Pharmacol. 2022 Jun:64:102230. doi: 10.1016/j.coph.2022.102230. Epub 2022 Apr 27.

Authors

Kyleigh A Rodgers¹, Kristina A Kigerl², Jan M Schwab³, Phillip G Popovich⁴

Affiliations

¹ Department of Neuroscience, The Ohio State University, Columbus, OH, USA; Medical Scientist Training Program, The Ohio State University, Columbus, OH, USA.
² Department of Neuroscience, The Ohio State University, Columbus, OH, USA; Center for Brain and Spinal Cord Repair, The Ohio State University, Columbus, OH, USA; The Belford Center for Spinal Cord Injury, The Ohio State University, Columbus, OH, USA.
³ Department of Neuroscience, The Ohio State University, Columbus, OH, USA; Medical Scientist Training Program, The Ohio State University, Columbus, OH, USA; Center for Brain and Spinal Cord Repair, The Ohio State University, Columbus, OH, USA; The Belford Center for Spinal Cord Injury, The Ohio State University, Columbus, OH, USA; Departments of Neurology and Physical Medicine and Rehabilitation, The Ohio State University, Columbus, OH 43210, USA.
⁴ Department of Neuroscience, The Ohio State University, Columbus, OH, USA; Medical Scientist Training Program, The Ohio State University, Columbus, OH, USA; Center for Brain and Spinal Cord Repair, The Ohio State University, Columbus, OH, USA; The Belford Center for Spinal Cord Injury, The Ohio State University, Columbus, OH, USA. Electronic address: phillip.popovich@osumc.edu.

Abstract

Infections impair neurological outcome and increase mortality after spinal cord injury (SCI). Emerging data show that pathogens more easily infect individuals with SCI because SCI disrupts neural and humoral control of immune cells, culminating with the development of "SCI-induced immune deficiency syndrome" (SCI-IDS). Here, we review data that implicate autonomic dysfunction and impaired neuroendocrine signaling as key determinants of SCI-IDS. Although it is widely appreciated that mature leukocyte dysfunction is a canonical feature of SCI-IDS, new data indicate that SCI impairs the development and mobilization of immune cell precursors in bone marrow. Thus, this review will also explore how the post-injury acquisition of a "bone marrow failure syndrome" may be the earliest manifestation of SCI-IDS.

Keywords: Adrenal glands; Bone marrow; Immune deficiency; Neuroendocrine; Neuroplasticity; Spinal cord injury; Spleen.

Publication types

Review
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Research Support, N.I.H., Extramural

MeSH terms

Bone Marrow
Humans
Immune System Diseases*
Signal Transduction
Spinal Cord Injuries*

Abstract

Publication types

MeSH terms

Grants and funding