Interleukin‐1‐induced neurotoxicity is mediated by glia and requires caspase activation and free radical release

Thornton, Peter; Pinteaux, Emmanuel; Gibson, Rosemary M.; Allan, Stuart M.; Rothwell, Nancy J.

doi:10.1111/j.1471-4159.2006.03872.x

Cited by 152

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Interleukin‐1‐induced neurotoxicity is mediated by glia and requires caspase activation and free radical release

Thornton, Peter, Pinteaux, Emmanuel, Gibson, Rosemary M., Allan, Stuart M., Rothwell, Nancy J.·2006·Journal of Neurochemistry

DOI 10.1111/j.1471-4159.2006.03872.x

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Abstract

Interleukin (IL)‐1 expression is induced rapidly in response to diverse CNS insults and is a key mediator of experimentally induced neuronal injury. However, the mechanisms of IL‐1‐induced neurotoxicity are unknown. The aim of the present study was to examine the toxic effects of IL‐1 on rat cortical cell cultures. Treatment with IL‐1β did not affect the viability of pure cortical neurones. However, IL‐1 treatment of cocultures of neurones with glia or purified astrocytes induced caspase activation resulting in neuronal death. Neuronal cell death induced by IL‐1 was prevented by pre‐treatment with the IL‐1 receptor antagonist, the broad spectrum caspase inhibitor Boc‐Asp‐(OMe)‐CH 2 F or the antioxidant α‐tocopherol. The NMDA receptor antagonist dizolcipine (MK‐801) attenuated cell death induced by low doses of IL‐1β but the α‐amino‐3‐hydroxy‐5‐methylisoxazole‐4‐propionic acid receptor antagonist 2,3‐dihydroxy‐6‐nitro‐7‐sulfamoyl‐benzo(F)quinoxaline (NBQX) had no effect. Inhibition of inducible nitric oxide synthase with N(ω)‐nitro‐l‐arginine methyl ester had no effect on neuronal cell death induced by IL‐1β. Thus, IL‐1 activates the IL‐1 type 1 receptor in astrocytes to induce caspase‐dependent neuronal death, which is dependent on the release of free radicals and may contribute to neuronal cell death in CNS diseases.

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The apparent lack of toxicity mediated by IL-1β compared to previous studies may be related to different experimental settings used, including concentrations and time of exposure to the cytokine.
“In addition, the apparent lack of toxicity mediated by IL-1β compared to previous studies [57, 58] may be related to different experimental settings used, including concentrations and time of exposure to the cytokine.”
From MT5-MMP promotes neuroinflammation, neuronal excitability and Aβ production in primary neuron/astrocyte cultures from the 5xFAD mouse model of Alzheimer’s disease (2022) · cites this paper as [57]

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10.1002/jnr.10142 · DOI
10.1038/nri1664 · DOI · Paper page
10.1016/0165-5728(90)90104-U · DOI
10.1523/JNEUROSCI.21-15-05528.2001 · DOI
10.1097/01.WCB.0000044631.80210.3C · DOI
10.4049/jimmunol.144.8.2999 · DOI · Paper page
10.1038/sj.bjp.0704382 · DOI
10.1016/0165-5728(93)90214-J · DOI
10.1007/BF03036448 · DOI
10.1002/(SICI)1098-1136(199911)28:2<114::AID-GLIA3>3.0.CO;2-O · DOI
10.1002/(SICI)1098-1136(20000215)29:4<347::AID-GLIA5>3.0.CO;2-8 · DOI
10.1016/j.jneuroim.2004.12.007 · DOI
10.1016/S0165-5728(03)00222-4 · DOI
10.1073/pnas.86.19.7611 · DOI · Paper page
10.1111/j.1460-9568.2005.04067.x · DOI
10.1159/000026433 · DOI
10.1002/glia.20109 · DOI
10.1016/S0092-8674(00)80434-1 · DOI · Paper page
10.1152/physrev.1999.79.4.1431 · DOI · Paper page
10.1159/000068322 · DOI
10.1083/jcb.85.3.890 · DOI
10.1523/JNEUROSCI.16-13-04080.1996 · DOI
10.1016/j.neulet.2004.10.069 · DOI
10.1046/j.1471-4159.2002.01184.x · DOI
10.1016/0361-9230(92)90033-T · DOI
10.1016/S0889-1591(02)00098-3 · DOI
10.1016/0165-6147(92)90047-A · DOI
10.1002/j.1460-2075.1991.tb07761.x · DOI
10.1046/j.1471-4159.2002.01178.x · DOI
10.1016/S0952-7915(01)00306-5 · DOI
Strijbos P. J., 1995, Interleukin‐1 beta attenuates excitatory amino acid‐induced neurodegeneration in vitro: involvement of nerve growth factor, J. Neurosci., 15, 3468, 10.1523/JNEUROSCI.15-05-03468.1995 · DOI
10.1523/JNEUROSCI.23-25-08692.2003 · DOI · Paper page

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Authors: Thornton, P., Pinteaux, E., Gibson, R. M., Allan, S. M., & Rothwell, N. J.
Venue: Journal of Neurochemistry
Publisher: Wiley
Published: 2006-05-30
Volume: 98
Issue: 1
Pages: 258-266
ISSN: 0022-3042
1471-4159
DOI: 10.1111/j.1471-4159.2006.03872.x
Cited by: 152
References: 0
Language: en
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor)

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Interleukin‐1‐induced neurotoxicity is mediated by glia and requires caspase activation and free radical release

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