scholarly journals Spinal cord injury-induced immune deficiency syndrome enhances infection susceptibility dependent on lesion level

Brain ◽  
2016 ◽  
Vol 139 (3) ◽  
pp. 692-707 ◽  
Author(s):  
Benedikt Brommer ◽  
Odilo Engel ◽  
Marcel A. Kopp ◽  
Ralf Watzlawick ◽  
Susanne Müller ◽  
...  
2019 ◽  
Vol 20 (15) ◽  
pp. 3762 ◽  
Author(s):  
James Hong ◽  
Alex Chang ◽  
Yang Liu ◽  
Jian Wang ◽  
Michael G. Fehlings

Spinal cord injury (SCI) is associated with an increased susceptibility to infections, such as pneumonia, which is the leading cause of death in these patients. This phenomenon is referred to as SCI immune deficiency syndrome (SCI-IDS), and has been shown to be more prevalent after high-level transection in preclinical SCI models. Despite the high prevalence of contusion SCIs, the effects of this etiology have not been studied in the context of SCI-IDS. Compared to transection SCIs, which involve a complete loss of supraspinal input and lead to the disinhibition of spinally-generated activity, contusion SCIs may cause significant local deafferentation, but only a partial disruption of sympathetic tone below the level of injury. In this work, we investigate the effects of thoracic (T6-7) and cervical (C6-7) moderate–severe contusion SCIs on the spleen by characterizing splenic norepinephrine (NE) and cortisol (CORT), caspase-3, and multiple inflammation markers at 3- and 7-days post-SCI. In contrary to the literature, we observe an increase in splenic NE and CORT that correspond to an increase in caspase-3 after thoracic SCI relative to cervical SCI. Further, we found differences in expression of leptin, eotaxin, IP-10, and IL-18 that implicate alterations in splenocyte recruitment and function. These results suggest that incomplete SCI drastically alters the level-dependence of SCI-IDS.


2017 ◽  
Vol 34 (24) ◽  
pp. 3407-3415 ◽  
Author(s):  
Caitlyn G. Katzelnick ◽  
Joseph P. Weir ◽  
Nancy D. Chiaravalloti ◽  
Glenn R. Wylie ◽  
Trevor A. Dyson-Hudson ◽  
...  

e-Neuroforum ◽  
2010 ◽  
Vol 16 (3) ◽  
Author(s):  
B. Brommer ◽  
M.A. Kopp ◽  
I. Laginha ◽  
J.M. Schwab

AbstractInfections are a leading cause of morbidi­ty and mortality in patients with acute spinal cord injury (SCI). It has recently become clear that SCI might increase susceptibility to infec­tion by central nervous system (CNS)-specific mechanisms: CNS injury induces a disrup­tion of the normally well-balanced interplay between the immune system and the CNS. As a result, SCI also leads to secondary im­munodeficiency (SCI injury-induced immu­nodepression, SCI-IDS) and infection. SCI-IDS (a) starts early after SCI (within 24 h), (b) af­fects both the innate and adaptive immune system, and (c) is independent of iatrogenic application of high-dose corticosteroids. The fact that increased immunosuppression cor­relates with lesion level underlines a neurogenic origin. Here we summarize the current understanding and main pathophysiological features of leukocyte dysfunction following SCI. A better understanding of this syndrome may provide insights into how the CNS controls the immune system. Furthermore, the identification of patients suffering from spi­nal cord injury as immunocompromised is a clinically relevant, yet widely underappreci­ated finding.


2003 ◽  
Vol 26 (1) ◽  
pp. 59-64 ◽  
Author(s):  
Craig J. Newsam ◽  
Audrey D. Lee ◽  
Sara J. Mulroy ◽  
Jacquelin Perry

2011 ◽  
Vol 122 (1) ◽  
pp. 163-170 ◽  
Author(s):  
H. Ogata ◽  
D.G. Sayenko ◽  
E. Yamamoto ◽  
T. Kitamura ◽  
S. Yamamoto ◽  
...  

1986 ◽  
Vol 73 (6) ◽  
pp. 590-598 ◽  
Author(s):  
B.M. Singh ◽  
S. Levine ◽  
R.L. Yarrish ◽  
M.J. Hyland ◽  
D. Jeanty ◽  
...  

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