Human astrocyte production of tumour necrosis factor-α, interleukin-1β, and interleukin-6 following exposure to lipopolysaccharide endotoxin

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

doi:10.1080/01616412.1993.11740119

Cited by 74 publications

(26 citation statements)

References 36 publications

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“…The first peak was TNF-a attributed to microglia and the second to astrocytes. Similar TNF-a response profiles have been reported in cultured microglia and astrocytes stimulated with lipopolysaccharide, 45,46 in traumatized brains, 47 and in the ischemic brain. 3 The magnitude of cellular TNF response to cerebral ischemia is animal strain dependent in the mouse, whereas the time-profile and the cellular sources of TNF are similar regardless of genetic background.…”

Section: Discussionsupporting

confidence: 61%

The effect of thalidomide on spinal cord ischemia/reperfusion injury in a rabbit model

et al. 2006

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Study design: Randomized study. Objectives: To evaluate the effects of thalidomide on spinal cord ischemia/reperfusion injury via reduced TNF-a production. Setting: Animal experimental laboratory, Clinical Research Institute of Seoul National University Hospital, Seoul, Korea. Methods: Spinal cord ischemia was induced in rabbits by occluding the infrarenal aorta. Rabbits in group N did not undergo ischemic insult, but rabbits in groups C (the untreated group), THA, and THB underwent ischemic insult for 15 min. The THA and THB groups received thalidomide (20 mg/kg) intraperitoneally (i.p.) before ischemia, but only the THB group received thalidomide (i.p., 20 mg/kg) after 24 and 48 h of reperfusion. After evaluating neurologic functions at 1.5 h, 3, and 5 days of reperfusion, rabbits were killed for histopathologic examination and Western blot analysis of TNF-a. Results: The THA and THB groups showed significantly less neurologic dysfunction than the C group at 1.5 h, 3, and 5 days of reperfusion. The number of normal spinal motor neurons in ventral gray matter was higher in THA and THB than in C, but no difference was observed between THA and THB. Western blot analysis showed a significantly higher level of TNF-a in C than in THA and THB at 1.5 h of reperfusion, but no difference was observed between C, THA, or THB at 3 or 5 days of reperfusion. Conclusion: Thalidomide treatment before ischemic insult reduces early phase ischemia/ reperfusion injury of the spinal cord in rabbits.

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Section: Discussionsupporting

confidence: 61%

The effect of thalidomide on spinal cord ischemia/reperfusion injury in a rabbit model

et al. 2006

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“…For example, TNF-␣ has been reported to provoke an anxiogenic response in the elevated plus maze test of anxiety in rodents (Connor et al 1998). In addition, whether our findings are relevant to trigger the cytokine cascade remains to be established, but it is very well known that among the proinflammatory cytokines, TNF-␣ exerts a special role since its activation switches on the process of synthesis of others such as IL1␣, IL1␤, IL6 and TNF-␣ itself in brain (Sharif et al 1993).…”

Section: Discussionmentioning

confidence: 99%

The Increase in TNF-α Levels Is Implicated in NF-κB Activation and Inducible Nitric Oxide Synthase Expression in Brain Cortex after Immobilization Stress

Madrigal

Hurtado

Moro

et al. 2002

Neuropsychopharmacology

219

120

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The underlying mechanisms by which physical or psychological stress causes neurodegeneration are still unknown. We have demonstrated that the high-output and long-lasting synthesizing source of nitric oxide (NO), inducible NO synthase (iNOS), is expressed in brain cortex after three weeks of repeated stress and that its overexpression accounts for the neurodegenerative changes found in this situation. Now we have found that a short duration of stress (immobilization for 6 h) also induces the expression of iNOS in brain cortex in adult male rats. In order to elucidate the possible mechanisms involved in iNOS expression, we have studied the role of the cytokine tumor necrosis factor-␣ (TNF-␣ ) released in brain during stress. We have shown that there is an increase in soluble TNF-␣ levels after 1 h of stress in cortex and that this is preceded by an increase in TNF-␣ -convertase (TACE) activity in brain cortex as soon as 30 min after immobilization. Stress-induced increase in both TACE activity and TNF-␣ levels seems to be mediated by excitatory amino acids since they can be blocked by MK-801 (dizocilpine) (0.2 mg/kg i.p.), an antagonist of the N-methyl-D-aspartate subtype of glutamate receptor. In order to study the role of TACE and TNF-␣ in iNOS induction, a group of animals were i.p. injected with the preferred TACE inhibitor BB1101 (2 and 10 mg/kg). Indeed, BB1101 inhibited iNOS expression induced by six hours of stress. In addition, we studied the role of the transcription factor nuclear factor B (NF-B), which is Gross and Wolin 1995). In this context, we have demonstrated that restrain stress induces a generalized increase in NO production (Leza et al. 1998) and that iNOS is expressed in brain cortex of rats exposed to stress (Olivenza et al. 2000). In support of the idea that iNOS is one of the mechanisms responsible for the functional damage in this condition, we have also demonstrated that aminoguanidine, a preferred inhibitor of iNOS, protects against cell damage produced by immobilization stress in rats (Olivenza et al. 2000; Madrigal et al. 2000), an experimental procedure used as a model of stress disorders in humans (Bremner et al. 1991).These evidences indicate that stress-induced iNOS expression in brain may mediate, at least in part, the anatomical and clinical features of neurotoxic damage found in animals and humans after exposure to uncontrollable stress (Sheline et al. 1996;Sapolsky 1996;Kim and Yoon 1998). This emphasizes the interest of the study of the mechanisms of iNOS expression after stress exposure. iNOS, as an inducible protein, is mainly regulated at the transcriptional level and is expressed after exposure of cells to several noxious agents such as cytokines and/or lipopolysaccharide (rev. in Nathan and Xie 1994). Although a considerable amount of evidence has shown that physical and psychological stress elevates plasma levels of several cytokines in animals and humans (i.e. TNF-␣ , IL-6, IFN ␥ ), the physiological significance of such elevation remains to be elucidated (Yamasu et a...

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“…Although astrocytes and neurons are capable of producing cytokines and NO (Sharif et al, 1993;Liu et al, 1994), activated microglia appear to be the major source of cytokines and NO in the injured central nervous system (Sawada et al, 1989;Lee et al, 1993;Lafortune et al, 1996). Cytokineinduced NO production requires GTP cyclohydrolase I (GTPCH).…”

Section: Introductionmentioning

confidence: 99%

Repression of proinflammatory cytokine and inducible nitric oxide synthase (NOS2) gene expression in activated microglia by N-acetyl-O-methyldopamine: Protein kinase a-dependent mechanism

Cho

Kim

Cruz

et al. 2001

Glia

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Human astrocyte production of tumour necrosis factor-α, interleukin-1β, and interleukin-6 following exposure to lipopolysaccharide endotoxin

Cited by 74 publications

References 36 publications

The effect of thalidomide on spinal cord ischemia/reperfusion injury in a rabbit model

The effect of thalidomide on spinal cord ischemia/reperfusion injury in a rabbit model

The Increase in TNF-α Levels Is Implicated in NF-κB Activation and Inducible Nitric Oxide Synthase Expression in Brain Cortex after Immobilization Stress

Repression of proinflammatory cytokine and inducible nitric oxide synthase (NOS2) gene expression in activated microglia by N-acetyl-O-methyldopamine: Protein kinase a-dependent mechanism

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