Early Expression and Cellular Localization of Proinflammatory Cytokines Interleukin-1β, Interleukin-6, and Tumor Necrosis Factor-α in Human Traumatic Spinal Cord Injury

Yang, Liqun; Blumbergs, Peter; Jones, Nigel R.; Manavis, Jim; Sarvestani, Ghafar T.; Ghabriel, M. N.

doi:10.1097/00007632-200405010-00004

Cited by 182 publications

(124 citation statements)

References 57 publications

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“…11,19 The reason for this difference might be that on top of an important function in the early inflammatory cascade, as shared with interleukin-1b and tumour necrosis factor-a, TGF-b1 is also involved in scar formation as previously shown in several experimental studies. 8,10,19 Lagord et al 8 proposed that TGF-b1 is mainly involved in the inflammatory reactions while TGF-b2 is involved in scar formation following crush injuries to the rat spinal cord.…”

Section: Discussionmentioning

confidence: 98%

TGF-β1 and TGF-β2 expression after traumatic human spinal cord injury

et al. 2007

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Study design: Immunohistochemical investigation in control and lesioned human spinal cords. Objectives: To assess the spatial and temporal expression patterns of transforming growth factor-b1 and -b2 (TGF-b1 and TGF-b2) in the human spinal cord after traumatic injury. Setting: Germany, Aachen, Aachen University Hospital. Methods: Sections from human spinal cords from 4 control patients and from 14 patients who died at different time points after traumatic spinal cord injury (SCI) were investigated immunohistochemically. Results: In control cases, TGF-b1 was confined to occasional blood vessels, intravascular monocytes and some motoneurons, whereas TGF-b2 was only found in intravascular monocytes. After traumatic SCI, TGF-b1 immunoreactivity was dramatically upregulated by 2 days after injury (the earliest survival time investigated) and was detected within neurons, astrocytes and invading macrophages. The staining was most intense over the first weeks after injury but gradually declined by 1 year. TGF-b2 immunoreactivity was first detected 24 days after injury. It was located in macrophages and astrocytes and remained elevated for up to 1 year. In white matter tracts undergoing Wallerian degeneration, there was no induction of either isoform. Conclusion: The early induction of TGF-b1 at the point of SCI suggests a role in the acute inflammatory response and formation of the glial scar, while the later induction of TGF-b2 may indicate a role in the maintenance of the scar. Neither of these TGF-b isoforms appears to contribute to the astrocytic scar formation in nerve fibre tracts undergoing Wallerian degeneration.

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Section: Discussionmentioning

confidence: 98%

TGF-β1 and TGF-β2 expression after traumatic human spinal cord injury

et al. 2007

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“…IL-1b, IL-6, IL-8, and TNF-a are considered to stimulate brain repair processes and astroglial scarring [3]. A previous autopsy study of traumatic spinal cord injury [31] indicated that IL-1b, IL-6, and TNF-a were detected in neurons 30 min after injury, indicating that the expression of these cytokines had declined sharply, returning to the baseline by 2 days after injury. This discrepancy of our data might be attributed to cross-sectional analysis of the inflammatory process or different types of nerve tissue injury/inflammation.…”

Section: Discussionmentioning

confidence: 99%

Tumor necrosis factor-α, interleukin-1β, and interleukin-6 in the cerebrospinal fluid of patients with cervical myelopathy and lumbar radiculopathy

et al. 2009

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There have been few reports describing cytokines in the cerebrospinal fluid (CSF) of patients with spinal degenerative disorders. This study investigated whether interleukin-1b (IL-1b), interleukin-6 (IL-6), and tumor necrosis factor-a (TNF-a) could be detected in CSF of patients with cervical myelopathy or lumbar radiculopathy and whether the concentrations of those cytokines correlated with the severity of disease conditions. CSF samples were obtained from 21 patients with cervical myelopathy (Group M) and 19 patients with lumbar radiculopathy (Group R), and six volunteers (control). The concentration of IL-6 was significantly higher in Groups M and R than in the control, possibly demonstrating spinal cord and nerve root damage, respectively. However, TNF-a was lower than the detection limit. IL-1b was detected in only five samples from three patients in Group M and two volunteers in the control. The concentrations of IL-6 did not show any correlation with symptom duration, the scoring system by the Japanese Orthopaedic Association, or the duration of nerve root block. There is a possibility that the concentration of inflammatory cytokines in CSF can indicate certain pathological aspects of cervical myelopathy or lumbar radiculopathy.

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“…Inflammatory processes characteristic of the acute stage of injury are likely to alter the actions of morphine. Pro-inflammatory cytokines, including interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α), are significantly upregulated 1, 3, and 6 hrs after a contusion injury, returning to background levels 1-2 days after injury [35,36]. Morphine appears to further increase pro-inflammatory cytokine levels by activating μ-receptors on spinal glial cells [37,38,39,40].…”

Section: Discussionmentioning

confidence: 99%

The impact of morphine after a spinal cord injury

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Washburn

et al. 2007

Behavioural Brain Research

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Nociceptive stimulation, at an intensity that elicits pain-related behavior, attenuates recovery of locomotor and bladder functions, and increases tissue loss after a contusion injury. These data imply that nociceptive input (e.g., from tissue damage) can enhance the loss of function after injury, and that potential clinical treatments, such pretreatment with an analgesic, may protect the damaged system from further secondary injury. The current study examined this hypothesis and showed that a potential treatment (morphine) did not have a protective effect. In fact, morphine appeared to exacerbate the effects of nociceptive stimulation. Experiment 1 showed that after spinal cord injury 20 mg/kg of systemic morphine was necessary to induce strong antinociception and block behavioral reactivity to shock treatment, a dose that was much higher than that needed for sham controls. In Experiment 2, contused rats were given one of three doses of morphine (Vehicle, 10, 20 mg/kg) prior to exposure to uncontrollable electrical stimulation or restraint alone. Despite decreasing nociceptive reactivity, morphine did not attenuate the long-term consequences of shock. Rats treated with morphine and shock had higher mortality rates, and displayed allodynic responses to innocuous sensory stimuli three weeks later. Independent of shock, morphine per se undermined recovery of sensory function. Rats treated with morphine alone also had significantly larger lesions than those treated with saline. These results suggest that nociceptive stimulation affects recovery despite a blockade of pain-elicited behavior. The results are clinically important because they suggest that opiate treatment may adversely affect the recovery of function after injury.

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Early Expression and Cellular Localization of Proinflammatory Cytokines Interleukin-1β, Interleukin-6, and Tumor Necrosis Factor-α in Human Traumatic Spinal Cord Injury

Cited by 182 publications

References 57 publications

TGF-β1 and TGF-β2 expression after traumatic human spinal cord injury

TGF-β1 and TGF-β2 expression after traumatic human spinal cord injury

Tumor necrosis factor-α, interleukin-1β, and interleukin-6 in the cerebrospinal fluid of patients with cervical myelopathy and lumbar radiculopathy

The impact of morphine after a spinal cord injury

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