Elevated Serum Titers of Proinflammatory Cytokines and CNS Autoantibodies in Patients with Chronic Spinal Cord Injury

Hayes, Keith C.; Hull, T.C.L.; Delaney, Gail A.; Potter, Patrick J.; Sequeira, Keith; Campbell, Kim; Popovich, Phillip G.

doi:10.1089/08977150260139129

Cited by 182 publications

(128 citation statements)

References 54 publications

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“…This results in the accumulation of stagnant urine within the bladder, allowing for an increase in bacterial growth and a resulting risk of infection. 2 UTIs have been consistently shown to be the most frequent cause of re-hospitalization in the SCI population, accounting for~24-54% of cases. 32 This indicates that UTIs are a common occurrence, not only during the acute stages of SCI but also in the long term as well.…”

Section: Somatic Nerve Damagementioning

confidence: 99%

“…As such, various areas of the body, particularly the gluteal and sacral regions, may be at risk for oxygen deprivation and necrosis. 2 Individuals with SCI are at a particularly high risk for pressure ulcer development with~40% of individuals developing a pressure sore within any three-year period. 32 Acute secondary health complications such as these result in an acute inflammatory response characterized by a spike in proinflammatory mediators.…”

Section: Somatic Nerve Damagementioning

confidence: 99%

“…This has been demonstrated by elevated levels of circulating proinflammatory cytokines and autoantibodies, which are apparent in individuals who are symptomatic or asymptomatic for secondary health complications. [1][2][3][4][5] As such, this population is often found to be in a perpetual low-grade inflammatory state, which is elevated to an even further extent when other health complications and associated disorders are present.…”

Section: Introductionmentioning

confidence: 99%

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Immune dysfunction and chronic inflammation following spinal cord injury

2014

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Study design: Review article. Objectives: The objective of this study is to provide an overview of the many factors that contribute to the chronic inflammatory state typically observed following spinal cord injury (SCI). Methods: Literature review. Results: Not applicable. Conclusion: SCI is typically characterized by a low-grade inflammatory state due to a number of factors. As bidirectional communication exists between the nervous, endocrine and immune systems, damage to the spinal cord may translate into both endocrinal and immune impairment. Damage to the autonomic nervous system may induce immune dysfunction directly, through the loss of neural innervation of lymphoid organs, or indirectly by inducing endocrinal impairment. In addition, damage to the somatic nervous system and the corresponding loss of motor and sensory function increases the likelihood of developing a number of secondary health complications and metabolic disorders associated with a state of inflammation. Lastly, numerous related disorders associated with a state of chronic inflammation have been found to be at a substantially higher prevalence following SCI. Together, such factors help explain the chronic inflammatory state and immune impairment typically observed following SCI. An understanding of the interactions between systems, both in health and disease, and the many causes of chronic inflammation may aid in the effective future treatment of immune dysfunction and related disorders following SCI.

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Section: Somatic Nerve Damagementioning

confidence: 99%

Section: Somatic Nerve Damagementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Immune dysfunction and chronic inflammation following spinal cord injury

2014

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“…The TNF-α levels were significantly elevated following an initial decrease in concentration in the first 12 h after injury. Although studies have shown increased IL-1β and TNF-α after SCI, 11,12 this was the first study to have taken repeated measurements over time to generate a temporal cytokine profile for IL-1β and TNF-α in humans. Because of the not especially large patient collective (n = 23), there were associated differences in absolute values with a high and variable s.d.…”

Section: Discussionmentioning

confidence: 99%

A pilot study on temporal changes in IL-1β and TNF-α serum levels after spinal cord injury: the serum level of TNF-α in acute SCI patients as a possible marker for neurological remission

Biglari¹,

Swing

Child

et al. 2015

Spinal Cord

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Study design: Serum levels of interleukin-1β (IL-1β) and tumour necrosis factor-α (TNF-α) were measured over a 12-week period in 23 patients with spinal cord injury (SCI) with and without neurological improvement. Objectives: To determine the course of IL-1β and TNF-α in patients with SCI and observe a possible relationship between improvements in neurological functioning and cytokine levels. Setting: All patients were treated at the BG Trauma Centre, Ludwigshafen, Germany. All lab work was done at the University Hospital, Heidelberg. Methods: Spinal cord injury was classified according to the American Spinal Injury Association (ASIA) impairment scale (AIS) in 23 patients. TNF-α and IL-1β levels were measured upon arrival at the hospital, after 4 h, 9 h and 12 h, on days 1 and 3 and at the end of weeks 1, 2, 4, 8 and 12. Results: Temporal changes in TNF-α and IL-1β in SCI patients were seen. Patients with AIS improvement (Group 1) had significantly lower TNF-α levels at 9 h compared with patients without AIS improvement (Group 2; Po0.01). The course of IL-1β fluctuated greatly between 4 h and week 1 in the groups; however, between 2 and 12 weeks post trauma, there was an overall decline in both groups. Conclusion: Measuring serum levels of TNF-α and IL-1β over time could be useful in tracking the course of SCI. Our data show differences in measured cytokines over a 12-week period for SCI patients with and without neurological improvement.

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“…52,53 Previously, it has been reported that cytokines induce the systemic overproduction of autoantibody. 54,55 In this context, the production of PGI 2 receptor-specific antibody might be called possibly, in part, an 'auto-immune' condition proved by injury to the spinal cord or related to secondary inflammatory conditions, such as, chronic pressure ulcers and/ or low grade infections of the bladder or respiratory tract.…”

Section: Similarity Of the Insulin And Pgi 2 Receptorsmentioning

confidence: 99%

Non-conventional hemostatic risk factors for coronary heart disease in individuals with spinal cord injury

et al. 2011

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Study design: Review. Objectives: In subjects with spinal cord injury (SCI), there is strong evidence for platelet hyperactivity, which may stimulate atherosclerosis and coronary heart disease (CHD). The literature was reviewed. Background: Individuals with SCI develop premature CHD. In addition to the conventional risk factors associated with CHD, there are pathologic hematological factors involved in atherogenesis that are similar to those that have been demonstrated in individuals with diabetes, and these hematological factors might affect individuals with SCI. One such hematological factor, platelet aggregation, is essential for the development of CHD, which results from thrombus formation in the coronary vasculature. Prostacyclin (PGI 2 ) is a potent inhibitor of platelet aggregation and is thought to have a beneficial role in inhibiting atherogenesis; therefore, it is possible that individuals with SCI have impaired PGI 2 receptor function. Methods: We reviewed the literature by conducting a search using PubMed (1970PubMed ( -2007. Results: Acute thrombosis is emerging as an important factor in the etiology of CHD and therefore could mediate the risk of CHD in persons with SCI, in addition to previously known risk factors such as hyperlipidemia, hypertension, hyperlipidemia, diabetes mellitus and hyperinsulinemia. Because PGI 2 may retard atherogenesis through its inhibitory effects on platelet function, we discuss the effects of PGI 2 on platelets in persons with SCI in this review. Conclusions Subjects with chronic SCI develop abnormal platelet function, resulting in the production of atherogenic and thrombogenic factors for the following reasons: (1) the PGI 2 and insulin receptors on their platelets are impaired; (2) thrombin generation and platelet-derived growth factor release are elevated; (3) insulin-induced nitric oxide production by platelets is markedly impaired; and (4) a circulating antibody (immunoglobulin G (IgG)) blocks the antithrombotic effect of both insulin and PGI 2 receptors. Thus, this IgG molecule is thought to be one of the pathological mediators of the increased incidence of CHD in individuals with SCI.

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Elevated Serum Titers of Proinflammatory Cytokines and CNS Autoantibodies in Patients with Chronic Spinal Cord Injury

Cited by 182 publications

References 54 publications

Immune dysfunction and chronic inflammation following spinal cord injury

Immune dysfunction and chronic inflammation following spinal cord injury

A pilot study on temporal changes in IL-1β and TNF-α serum levels after spinal cord injury: the serum level of TNF-α in acute SCI patients as a possible marker for neurological remission

Non-conventional hemostatic risk factors for coronary heart disease in individuals with spinal cord injury

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