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Our research aims to understand the underlying mechanism of the maladaptive immune response triggered by spinal cord injury (SCI). SCI has been associated with both systemic immune deficiency syndrome and post-traumatic autoimmunity. Both maladaptive neuro-immunological syndromes are associated with inferior repair and serve as a target to improve neurological recovery. We apply a bedside to benchside translational approach to investigate clinical symptoms with molecular techniques in order to develop novel treatments for patients suffering from spinal cord injury.


The central nervous system (CNS) and the immune system are integrated supersystems that regulate physiological homeostasis. Although the CNS is normally immune privileged, upon injury, the immune system enters the CNS to clear debris and stimulate repair. Unfortunately, once the homeostasis is disrupted between these two systems, they can have detrimental effects on each other. Most research studying the immune system after SCI has focused on understanding the function of leukocytes at the site of injury. However, injury to the spinal cord also disrupts the CNS control over the immune system and endocrine organs. This disruption of the sympathetic nervous system leads to a condition known as spinal cord injury-induced immune depression syndrome (SCI-IDS) (Riegger et al., 2003, 2007, 2009). This means that immune suppression after SCI is partly “neurogenic” (originating from the nervous system). Neurogenic SCI-IDS is functionally relevant and propagates the susceptibility of infection in a lesion level dependent manner. Among paraparetic animals the bacterial load in the lung increases with lesion level height using a controlled model of experimental pneumonia (Brommer et al., 2016). A maladaptive neuroendocrine reflex has been identified as a major neurogenic cause which occurs in a lesion level dependent manner and results in elevated susceptibility for infections (pneumonia) (Prüss et al., 2017)  Non-neurogenic mechanisms of immunosuppression also exist, including “systemic immune response syndrome” (SIRS) and “compensatory anti-inflammatory response syndrome” (CARS), which are triggered by injury, partly induced by the rapid apoptotic cell death in primary and secondary lymphoid organs. Together, both SCI-IDS and SIRS/CARS make the patient highly susceptible to infections, which are the leading cause of death after acute SCI and have also been shown to reduce neurological and functional recovery (Failli et al., 2012, Kopp et al., 2017).




In addition to immune suppression, there are also reports of SCI patients developing autoimmunity, making the interplay between these two systems more complex. Despite the reductions in systemic immunity, in the lesioned spinal cord local non-resolving inflammation occurs. This sustained inflammation leads to neurodegeneration, demyelination, and autoimmunity. This autoimmunity can be associated with maladaptive axonal plasticity, leading to pain and preventing functional recovery.




Local and systemic immune dysfunction occur acutely after SCI and persist into the chronic phase of SCI, comprising a substrate for propagated neurodegeneration. (Schwab et al., 2014).  

Although seemingly paradoxical, the systemic and localized immune dysfunctions are interdependent. SCI-IDS limits excessive autoimmunity (e.g. MS), but also leaves patients vulnerable to infections. These infections generate excessive host and pathogen-specific RNA, DNA, and cellular debris, all of which are immunogenic and serve as adjuvants to boost inflammation in the injured spinal cord. Additionally, pathogen-associated molecular patterns (PAMPs) are able to bind to Toll-like receptors (TLRs) (Akira et al., 2006) expressed on neurons, astrocytes, microglia, and oligodendrocytes. This infection-derived ligand recognition by TLRs is a possible mechanism for mediating neuronal injury and autoimmunity.


Topics and ongoing projects

  1. Spinal Cord Injury-induced Immune Depression Syndrome (SCI-IDS)

SCI disrupts the interplay between the immune system and the CNS (Meisel et al., 2005), leaving patients vulnerable to infections such as pneumonia and urinary tract infections. Patients with acute SCI who suffer from infections have a worse prognosis for neurological repair. Our lab is interested in understanding the triggers and implications of the immunodepression syndrome induced by SCI. Using different models of SCI and pneumonia, we can investigate what functional deficits result from infection after SCI and explore the underlying mechanisms for these deficits. The impact of acquired infections on secondary damage to the nervous system and intrinsic recovery potential is under investigation. Our lab strives to identify novel clinical strategies to combat SCI-IDS, using a bench-to-bedside and bedside-to-bench approach.


  1. Spinal Cord Injury-induced autoimmunity

Another aspect of the maladaptive immune response after SCI is SCI-induced autoimmunity. Despite systemic reductions in immunity, at the site of injury there is non-resolving inflammation (Prüss et al., 2011). This ongoing inflammation causes maladaptive priming of lymphocytes against self-antigens. We are interested in understanding the presence and function of these autoreactive T- and B-cells after SCI.



After acute SCI, T-cells become encephalitogenic and invade the CNS through the blood spinal cord barrier (BSB) (A, Popovich et al., 1996). Similarly, B-cells form follicular-like structures in areas adjacent to the lesion site after SCI (B,. Schwab et al., 2014.)


  1. Hypoxia and mitochondrial disruption after SCI

Together these altered immune responses leave SCI patients vulnerable to secondary damage. In particular, high amounts of hypoxia and mitochondrial damage are observed acutely after SCI. We are interested in understanding these conditions at chronic timepoints after SCI.

The Schwab Lab is affiliated with the Belford Center for Spinal Cord Injury and the Center for Brain and Spinal Cord Repair (CBSCR) at the Ohio State University. 


Clinical trials

  • Design and conduction of diagnostic and interventional mono-/and multicentric randomized trials in patients following spinal cord injury.

Experimental models

  • SCI-models (contusion, transection) in mice & rats.
  • Experimental pneumonia model (Streptococcus pneumoniae)

Cell and molecular biology

  • Gene expression analysis (qPCR, Western Blot)
  • FACS analysis
  • Immunohistochemistry- paraffin-embed tissue (Single and double labeling)
  • Immunohistochemistry- cryopreserved tissue (Fluorescent labeling)
  • Cell culture


  • Behavioral testing (e.g. catwalk, BBB)


Akira S, Uematsu S, Takeuchi O (2006). Pathogen Recognition and Innate Immunity. Cell 124:783-801.

Brommer B, Engel O, Kopp MA, Watzlawick R, Müller S, Prüss H, Chen Y, DeVivo MJ, Finkenstaedt FW, Dirnagl U, Liebscher T, Meisel A, Schwab JM (2017). Spinal cord injury-induced immune deficiency syndrome enhances infection susceptibility dependent on lesion level. Brain 139:692-707.

Failli V, Kopp MA, Gericke C, Martus P, Klingbeil S, Brommer B, Laginha I, Chen Y, DeVivo MJ, Dirnagl U, Schwab JM (2012). Functional neurological recovery after spinal cord injury is impaired in patients with infections. Brain 135:3238-3250.

Kopp MA, Watzlawick R, Martus P, Failli V, Finkenstaedt FW, Chen Y, DeVivo MJ, Dirnagl U, Schwab JM (2017). Long-term functional outcome in patients with acquired infections after acute spinal cord injury. Neurology 28;88:892-900.

Meisel C, Schwab JM, Prass K, Meisel A, Dirnagl U (2005). Central nervous system injury-induced immune deficiency syndrome. Nature Reviews Neuroscience 6:775-786.

Popovich P, Stokes B, Whitacre C (1996). Concept of autoimmunity following spinal cord injury: Possible roles for T lymphocytes in the traumatized central nervous system. Journal of Neuroscience Research 45:349-363.

Prüss H, Kopp MA, Brommer B, Gatzemeier N, Laginha I, Dirnagl U, Schwab JM (2011). Non-Resolving Aspects of Acute Inflammation after Spinal Cord Injury (SCI): Indices and Resolution Plateau. Brain Pathology 21:652-660.

Prüss H, Tedeschi A, Thiriot A, Lynch L, Loughead SM, Stutte S, Mazo IB, Kopp MA, Brommer B, Blex C, Geurtz LC, Liebscher T, Niedeggen A, Dirnagl U, Bradke F, Volz MS, DeVivo MJ, Chen Y, von Andrian UH, Schwab JM (2017). Spinal cord injury-induced immunodeficiency is mediated by a sympathetic-neuroendocrine adrenal reflex. Nature Neuroscience 20(11):1549-1559

Riegger T, Conrad S, Liu K, Schluesener HJ, Adibzahdeh M, Schwab JM (2007). Spinal cord injury-induced immune depression syndrome (SCI-IDS). Eur J Neurosci 25 :1743-7.

Riegger T, Conrad S, Schluesener HJ, Kaps HP, Badke A, Baron C, Gerstein J, Dietz K, Abdizahdeh M, Schwab JM (2009). Immune depression syndrome following human spinal cord injury (SCI): a pilot study. Neuroscience 158:1194-9.

Riegger T, Schluesener HJ, Conrad S, et al (2003). Hematologic Cellular Inflammatory Response Following Human Spinal Cord Injury: 48th Annual Meeting of the German Society for Neuropathology and Neuroanatomy. Berlin: Acta Neuropathol 392.

Schwab JM, Brechtel K, Muellera C, Failli V, Kaps H, Tuli SK, Schluesener HJ (2006). Experimental strategies to promote spinal cord regeneration—an integrative perspective. Progress in Neurobiology 78:91-116.

Schwab JM, Zhang Y, Kopp MA, Brommer B, Popovich PG (2014). The paradox of chronic neuroinflammation, systemic immune suppression, autoimmunity after traumatic chronic spinal cord injury. Experimental Neurology 258:121-129.