Traumatic injury induces interleukin-6 production by human astrocytes

Hariri, Robert; Chang, Victor; Barie, Philip S.; Wang, Ruby S.; Sharif, Setareh F.; Ghajar, Jam

doi:10.1016/0006-8993(94)90188-0

Cited by 71 publications

(32 citation statements)

References 21 publications

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“…In this regard, several findings have specifically demonstrated a protective role of neuronal TNF-a against excitotoxicity induced by glutamate receptor agonists (Allan, 2002) or nitric oxide (Turrin and Rivest, 2006), although we have previously shown that aged rats show a slower progression of neurodegeneration to NMDA-induced excitotoxicity than adult rats (Castillo-Ruiz et al, 2007), occurring concomitantly to the expression of TNF-a in neuronal cells of the LC, when overall levels are lower than in the adult. In regard to IL-6, adult striatal values are increased from 6 hr to 5 dpl in neurons, astrocytes and microglial cells, as previously reported (Ali et al, 2000;Hariri et al, 1994;Orzylowska et al, 1999;Schiefer et al, 1998;Suzuki et al, 1999aSuzuki et al, , 1999b. In contrast, in the aged striatum we report higher expression levels at all survival times, and an injury-induced early up-regulation at 6 hr after lesioning, partly occurring in neuronal cells.…”

Section: Injury-induced Cytokine Response Is Attenuated In the Aged Bsupporting

confidence: 86%

Increased levels of proinflammatory cytokines in the aged rat brain attenuate injury‐induced cytokine response after excitotoxic damage

Campuzano

Castillo-Ruiz

Acarín

et al. 2009

J of Neuroscience Research

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In order to evaluate proinflammatory cytokine levels and their producing cell types in the control aged rat brain and after acute excitotoxic damage, both adult and aged male Wistar rats were injected with N-methyl-D-aspartate in the striatum. At different survival times between 6 hr and 7 days after lesioning, interleukin-1 beta (IL-1beta), interleukin-6 (IL-6), and tumor necrosis factor alpha (TNF-alpha) were analyzed by enzyme-linked immunosorbent assay and by double immunofluorescence of cryostat sections by using cell-specific markers. Basal cytokine expression was attributed to astrocytes and was increased in the normal aged brain showing region specificity: TNF-alpha and IL-6 displayed age-dependent higher levels in the aged cortex, and IL-1beta and IL-6 in the aged striatum. After excitotoxic striatal damage, notable age-dependent differences in cytokine induction in the aged vs. the adult were seen. The adult injured striatum exhibited a rapid induction of all cytokines analyzed, but the aged injured striatum showed a weak induction of cytokine expression: IL-1beta showed no injury-induced changes at any time, TNF-alpha presented a late induction at 5 days after lesioning, and IL-6 was only induced at 6 hr after lesioning. At both ages, in the lesion core, all cytokines were early expressed by neurons and astrocytes, and by microglia/macrophages later on. However, in the adjacent lesion border, cytokines were found in reactive astrocytes. This study highlights the particular inflammatory response of the aged brain and suggests an important role of increased basal levels of proinflammatory cytokines in the reduced ability to induce their expression after damage.

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Section: Injury-induced Cytokine Response Is Attenuated In the Aged Bsupporting

confidence: 86%

Increased levels of proinflammatory cytokines in the aged rat brain attenuate injury‐induced cytokine response after excitotoxic damage

Campuzano

Castillo-Ruiz

Acarín

et al. 2009

J of Neuroscience Research

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“…However, a detailed mechanism of the immune system in the brain has not been elucidated. Recent reports have demonstrated that astrocytes and microglia in the brain are capable of secreting IL-6 [12,32], in addition to a wide variety of cells including endothelial cells, monocytes/macrophages, T and B cells, and fibroblasts. Additionally, brain tumours such as acoustic neurinomas or meningiomas secrete IL-6 themselves and may act as an autocrine factor in controlling tumour growth [1,26].…”

Section: Discussionmentioning

confidence: 99%

Changes in serum cytokine concentrations after neurosurgical procedures

et al. 1996

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Cytokine responses to surgical trauma have been studied in 70 patients undergoing various neurosurgical procedures. Serum concentrations of interleukin-1 beta (IL-1 beta), interleukin-6 (IL-6), interleukin-8, (IL-8), tumour necrosis factor-alpha (TNF-alpha), and interferon-gamma (IFN-gamma) were measured before and after surgery using enzyme-linked immunosorbent assays. The serum concentrations of IL-1 beta, IL-8, TNF-alpha, and IFN-gamma did not change significantly following neurosurgical operations. In contrast, serum IL-6 levels were significantly elevated following surgery, peaking at postoperative day 1 and then gradually decreasing. Maximum IL-6 concentrations were considerably higher in patients who underwent surgery for brain tumours or aneurysms as compared with patients who had a ventriculoperitoneal shunt, neurovascular decompression or transsphenoidal adenomectomy. Intra-operative use of methylprednisolone, which is known to block the production and action of cytokines, suppressed the increase in IL-6 levels after surgery. There was a statistically significant correlation between the IL-6 peak concentration and the length of surgery in patients not treated with steroids, but not in patients treated with steroids. Additionally patients who underwent supratentorial surgery had higher peak concentrations of IL-6 than those who underwent infratentorial surgery. These results suggest that IL-6 is an early marker of tissue damage and may be useful in assessing the extent of postoperative stress.

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“…Cells of many types can synthesize IL-6 usually at low basal level with local induction in inflamed or traumatized tissue. In the CNS, astrocytes and microglial cells are recognized sources of IL-6 and expression of the IL-6 gene is increased by injury (Woodroofe et al, 1991;Van et al, 1992;Kiefer et al, 1993;Hariri et al, 1994;Shohami et al, 1994). IL-6 mRNA has been described within hippocampal and cerebellar neurons of the adult mammalian brain (Schiibitz et al, 1993).…”

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confidence: 99%

Induction of interleukin-6 in axotomized sensory neurons

et al. 1995

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RNA from rat dorsal root ganglia was analyzed in search of potentially beneficial cytokines that are induced in dorsal root ganglia by nerve injury. By reverse transcription, the PCR, and Southern blotting, interleukin-6 mRNA was detected during development but not in normal adult dorsal root ganglia, reappeared within 1 d of sciatic nerve transection, was maximally increased after 2 and 4 d, and decreased below the threshold of detection within 1 week. By RNase protection assay, interleukin-6 mRNA was consistently present in RNA from dorsal root ganglia removed from rats 4 d following transection but not in control dorsal root ganglia. Interleukin-6 bioactivity was also present in dorsal root ganglia following nerve injury. By in situ hybridization, interleukin-6 mRNA was localized within large and medium- sized axotomized neurons. In summary, some sensory neurons respond to axotomy with a brisk transient increase in synthesis of interleukin-6. Injury to the sciatic nerve also induced mRNAs for interleukin-1 beta and tumor necrosis factor-alpha in dorsal root ganglia. The inductions of interleukin-1 beta and tumor necrosis factor-alpha mRNAs were later and more sustained than that of interleukin-6 mRNA. The cellular sources of these two cytokines have not been defined.

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Traumatic injury induces interleukin-6 production by human astrocytes

Cited by 71 publications

References 21 publications

Increased levels of proinflammatory cytokines in the aged rat brain attenuate injury‐induced cytokine response after excitotoxic damage

Increased levels of proinflammatory cytokines in the aged rat brain attenuate injury‐induced cytokine response after excitotoxic damage

Changes in serum cytokine concentrations after neurosurgical procedures

Induction of interleukin-6 in axotomized sensory neurons

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