scholarly journals Spinal Cord Injury Increases Pro-inflammatory Cytokine Expression in Kidney at Acute and Sub-chronic Stages

Inflammation ◽  
2021 ◽  
Author(s):  
Shangrila Parvin ◽  
Clintoria R. Williams ◽  
Simone A. Jarrett ◽  
Sandra M. Garraway
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Inflammatory Response ◽  
Inflammatory Cytokine ◽  
Cardiovascular Health ◽  
Mrna Levels ◽  
Post Injury ◽  
Cord Injury ◽  
And Function ◽  
The Impact

Abstract— Accumulating evidence supports that spinal cord injury (SCI) produces robust inflammatory plasticity. We previously showed that the pro-inflammatory cytokine tumor necrosis factor (TNF)α is increased in the spinal cord after SCI. SCI also induces a systemic inflammatory response that can impact peripheral organ functions. The kidney plays an important role in maintaining cardiovascular health. However, SCI-induced inflammatory response in the kidney and the subsequent effect on renal function have not been well characterized. This study investigated the impact of high and low thoracic (T) SCI on C-fos, TNFα, interleukin (IL)-1β, and IL-6 expression in the kidney at acute and sub-chronic timepoints. Adult C57BL/6 mice received a moderate contusion SCI or sham procedures at T4 or T10. Uninjured mice served as naïve controls. mRNA levels of the proinflammatory cytokines IL-1β, IL-6, TNFα, and C-fos, and TNFα and C-fos protein expression were assessed in the kidney and spinal cord 1 day and 14 days post-injury. The mRNA levels of all targets were robustly increased in the kidney and spinal cord, 1 day after both injuries. Whereas IL-6 and TNFα remained elevated in the spinal cord at 14 days after SCI, C-fos, IL-6, and TNFα levels were sustained in the kidney only after T10 SCI. TNFα protein was significantly upregulated in the kidney 1 day after both T4 and T10 SCI. Overall, these results clearly demonstrate that SCI induces robust systemic inflammation that extends to the kidney. Hence, the presence of renal inflammation can substantially impact renal pathophysiology and function after SCI.

scholarly journals A geospatial examination of specialist care accessibility and impact on health outcomes for patients with acute traumatic spinal cord injury in NSW, Australia: a whole population record linkage study

2020 ◽  
Author(s):  
Lisa Nicole Sharwood ◽  
Bharat P Vaikuntam ◽  
Christiana L Cheng ◽  
Vanessa Noonan ◽  
Anthony P Joseph ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Record Linkage ◽  
Linkage Study ◽  
Traumatic Spinal Cord Injury ◽  
Specialist Care ◽  
Post Injury ◽  
Cord Injury ◽  
The Right ◽  
The Impact

Background Timely treatment is essential for achieving optimal outcomes after traumatic spinal cord injury (TSCI), and expeditious transfer to a specialist spinal cord injury unit (SCIU) is recommended within 24 hours from injury. Previous research in New South Wales (NSW) found only 57% of TSCI patients were admitted to SCIU for acute post-injury care; 73% transferred within 24 hours from injury. Methods This record linkage study included administrative pre-hospital, admissions and costs data for all patients aged ≥16 years with incident TSCI in NSW (2013-2016). Its aim was to examine potential geographical disparities in access to specialist care following TSCI using geospatial methods, and to better understand the impact of post-injury care pathways on patient outcomes. Results Of 316 cases with geospatial data, injury location analysis showed that over half (53%, n=168) of all patients were injured within 60 minutes road travel of a SCIU, yet only 28.6% (n=48) were directly transferred to a SCIU. Direct transfers received earlier operative intervention (median (IQR) 12.9(7.9) hours), compared with patients transferred indirectly to SCIU (median (IQR) 19.5(18.9) hours), and had lower risk of complications (OR 3.2 v 1.4, p<0.001). Conclusions Getting patients with acute TSCI patients to the right place at the right time is dependent on numerous factors; some are still being triaged directly to non-trauma services which delays specialist and surgical care and increases complication risks. More stringent adherence to recommended guidelines would prioritise direct SCIU transfer for patients injured within 60 minutes radius, enabling the benefits of specialised care.   

scholarly journals Splenic sympathetic signaling contributes to acute neutrophil infiltration of the injured spinal cord

2020 ◽  
Vol 17 (1) ◽  
Author(s):  
Susana Monteiro ◽  
Andreia G. Pinho ◽  
Mara Macieira ◽  
Cláudia Serre-Miranda ◽  
Jorge R. Cibrão ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Inflammatory Response ◽  
Neutrophil Infiltration ◽  
Innate Immune ◽  
Injured Spinal Cord ◽  
Post Injury ◽  
Cord Injury ◽  
Immune Changes

Abstract Background Alterations in the immune system are a complication of spinal cord injury (SCI) and have been linked to an excessive sympathetic outflow to lymphoid organs. Still unknown is whether these peripheral immune changes also contribute for the deleterious inflammatory response mounted at the injured spinal cord. Methods We analyzed different molecular outputs of the splenic sympathetic signaling for the first 24 h after a thoracic compression SCI. We also analyzed the effect of ablating the splenic sympathetic signaling to the innate immune and inflammatory response at the spleen and spinal cord 24 h after injury. Results We found that norepinephrine (NE) levels were already raised at this time-point. Low doses of NE stimulation of splenocytes in vitro mainly affected the neutrophils’ population promoting an increase in both frequency and numbers. Interestingly, the interruption of the sympathetic communication to the spleen, by ablating the splenic nerve, resulted in reduced frequencies and numbers of neutrophils both at the spleen and spinal cord 1 day post-injury. Conclusion Collectively, our data demonstrates that the splenic sympathetic signaling is involved in the infiltration of neutrophils after spinal cord injury. Our findings give new mechanistic insights into the dysfunctional regulation of the inflammatory response mounted at the injured spinal cord.

Cardiac consequences of spinal cord injury: systematic review and meta-analysis

Heart ◽  
2018 ◽  
Vol 105 (3) ◽  
pp. 217-225 ◽  
Author(s):  
Alexandra Mackenzie Williams ◽  
Cameron Marshall Gee ◽  
Christine Voss ◽  
Christopher Roy West
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Diastolic Function ◽  
Data Extraction ◽  
Meta Analysis ◽  
Left Ventricular ◽  
Structure And Function ◽  
Cord Injury ◽  
And Function ◽  
The Impact

ObjectiveConduct a meta-analysis to determine the impact of traumatic spinal cord injury (SCI) on echocardiographic measurements of left ventricular (LV) structure and function.MethodsMEDLINE and Embase were used for primary searches of studies reporting LV echocardiographic data in individuals with SCI. Of 378 unique citations, 36 relevant full-text articles were retrieved, and data from 27 studies were extracted for meta-analyses. Literature searches, article screening and data extraction were completed by two independent reviewers and compared for agreement. Primary analyses compared echocardiographic indices between individuals with SCI and able-bodied individuals, using a random effects model.ResultsData are reported as pooled effect estimates (95% CI). Data from 22 articles (474 participants) were included in the primary meta-analysis. Compared with able-bodied individuals, individuals with SCI had reductions to LV stroke volume of 11.8 mL (95% CI −17.8 to −5.9, p<0.001), end-diastolic volume of 19.6 mL (95% CI −27.2 to −11.9, p<0.001) and LV massindex of −7.7 g/m2 (95% CI −11.6 to −3.8, p<0.001), but ejection fraction was not different between the groups (95% CI −2.6% to 0.6%, p=0.236). Individuals with SCI also had altered indices of diastolic function, specifically a lowered ratio of early-to-late filling velocities (p=0.039), and augmented ratio of early diastolic flow-to-tissue velocities (p=0.021).ConclusionsIndividuals with SCI have smaller LV volumes and mass, and altered systolic and diastolic function. While this meta-analysis demonstrates important alterations to echocardiographic measures of cardiac structure and function at rest, future work should consider the impacts of SCI on the heart’s capacity or ‘reserve’ to respond to physiological challenges.PROSPERO registration numberCRD42017072333.

Differential expression of metabolic genes essential for glucose and lipid metabolism in skeletal muscle from spinal cord injured subjects

2011 ◽  
Vol 110 (5) ◽  
pp. 1204-1210 ◽  
Author(s):  
Yun Chau Long ◽  
Emil Kostovski ◽  
Hanneke Boon ◽  
Nils Hjeltnes ◽  
Anna Krook ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Mrna Levels ◽  
Metabolic Gene ◽  
Metabolic Gene Expression ◽  
Cord Injury ◽  
The Impact ◽  
Spinal Cord Injured

Skeletal muscle plays an important role in the regulation of energy homeostasis; therefore, the ability of skeletal muscle to adapt and alter metabolic gene expression in response to changes in physiological demands is critical for energy balance. Individuals with cervical spinal cord lesions are characterized by tetraplegia, impaired thermoregulation, and altered skeletal muscle morphology. We characterized skeletal muscle metabolic gene expression patterns, as well as protein content, in these individuals to assess the impact of spinal cord injury on critical determinants of skeletal muscle metabolism. Our results demonstrate that mRNA levels and protein expression of skeletal muscle genes essential for glucose storage are reduced, whereas expression of glycolytic genes is reciprocally increased in individuals with spinal cord injury. Furthermore, expression of genes essential for lipid oxidation is coordinately reduced in spinal cord injured subjects, consistent with a marked reduction of mitochondrial proteins. Thus spinal cord injury resulted in a profound and tightly coordinated change in skeletal muscle metabolic gene expression program that is associated with the aberrant metabolic features of the tissue.

MiRNA-194-5p inhibits inflammatory response after spinal cord injury via regulating TRAF6

2020 ◽  
Vol 111 (6) ◽  
Author(s):  
Siyuan Chen ◽  
Jinsong Wei ◽  
Liumei Huang ◽  
Bolin Feng ◽  
Weixiong Guo
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Inflammatory Response ◽  
Cord Injury

scholarly journals D-dopachrome tautomerase activates COX2/PGE2 pathway of astrocytes to mediate inflammation following spinal cord injury

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Huiyuan Ji ◽  
Yuxin Zhang ◽  
Chen Chen ◽  
Hui Li ◽  
Bingqiang He ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Signal Pathways ◽  
Post Injury ◽  
Dopachrome Tautomerase ◽  
Protein Levels ◽  
Cytokines And Chemokines ◽  
Cord Injury ◽  
Mitogen Activated Protein ◽  
Spinal Cord Contusion

Abstract Background Astrocytes are the predominant glial cell type in the central nervous system (CNS) that can secrete various cytokines and chemokines mediating neuropathology in response to danger signals. D-dopachrome tautomerase (D-DT), a newly described cytokine and a close homolog of macrophage migration inhibitory factor (MIF) protein, has been revealed to share an overlapping function with MIF in some ways. However, its cellular distribution pattern and mediated astrocyte neuropathological function in the CNS remain unclear. Methods A contusion model of the rat spinal cord was established. The protein levels of D-DT and PGE2 synthesis-related proteinase were assayed by Western blot and immunohistochemistry. Primary astrocytes were stimulated by different concentrations of D-DT in the presence or absence of various inhibitors to examine relevant signal pathways. The post-injury locomotor functions were assessed using the Basso, Beattie, and Bresnahan (BBB) locomotor scale. Results D-DT was inducibly expressed within astrocytes and neurons, rather than in microglia following spinal cord contusion. D-DT was able to activate the COX2/PGE2 signal pathway of astrocytes through CD74 receptor, and the intracellular activation of mitogen-activated protein kinases (MAPKs) was involved in the regulation of D-DT action. The selective inhibitor of D-DT was efficient in attenuating D-DT-induced astrocyte production of PGE2 following spinal cord injury, which contributed to the improvement of locomotor functions. Conclusion Collectively, these data reveal a novel inflammatory activator of astrocytes following spinal cord injury, which might be beneficial for the development of anti-inflammation drug in neuropathological CNS.

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