Immunoreactive interleukin-1β localization in the rat forebrain

Lechan, Ronald M.; Toni, Roberto; Clark, Burton D.; Cannon, Joseph G.; Shaw, Alan; Dinarello, Charles A.; Reichlin, Seymour

doi:10.1016/0006-8993(90)90445-h

Cited by 347 publications

(133 citation statements)

References 32 publications

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“…IL-1␤ is synthesized by neuronal and glial cells (Lechan et al, 1990) and is released in response to injury, insult, and stress (Benveniste, 1992;Bhat et al, 1996;Bartholdi and Schwab, 1997;Dinarello, 2004aDinarello, , 2006. We found that spinal cord neurons, which are generally not associated with immune functions, express NALP1 inflammasome proteins.…”

Section: Discussionmentioning

confidence: 80%

A Molecular Platform in Neurons Regulates Inflammation after Spinal Cord Injury

Vaccari¹,

Lotocki²,

Marcillo³

et al. 2008

J. Neurosci.

308

334

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Section: Discussionmentioning

confidence: 80%

A Molecular Platform in Neurons Regulates Inflammation after Spinal Cord Injury

Vaccari¹,

Lotocki²,

Marcillo³

et al. 2008

J. Neurosci.

308

334

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“…These effects include modulation of thermoregulation, sleep, and appetite, which are perhaps consistent with the relatively high expression of the signal-generating IL-1 type 1 receptors (IL-1R1) in hypothalamus (1)(2)(3)(4)(5). However, IL-1␤ also inhibits transmitter release (6,7) and calcium channel activity (7,8) in the hippocampus, and it has been shown to inhibit long term potentiation (LTP) in CA1, CA3, and dentate gyrus in vitro (9 -11) and in dentate gyrus in vivo (12)(13)(14)(15); these effects are consistent with the high distribution of IL-1R1 in hippocampus (1)(2)(3)(4)(5). The inhibitory effects of IL-1␤ in hippocampus have been linked with stimulation of the stress-activated kinases, p38 and JNK (14,16), which have also been shown to be activated by IL-1␤ in other cells (17)(18)(19)(20).…”

Section: Interleukin-1␤ (Il-1␤)mentioning

confidence: 71%

The Anti-inflammatory Cytokine, Interleukin (IL)-10, Blocks the Inhibitory Effect of IL-1β on Long Term Potentiation

Kelly

Lynch

Vereker

et al. 2001

Journal of Biological Chemistry

127

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Several effects of the proinflammatory cytokine, interleukin-1␤ (IL-1␤), have been described in the central nervous system, and one area of the brain where marked changes have been reported is the hippocampus. Among these changes are an IL-1␤-induced inhibition of long term potentiation (LTP) in perforant path-granule cell synapses and an attenuation of glutamate release in synaptosomes prepared from the hippocampus. Evidence suggests that, at least in circulating cells, the anti-inflammatory cytokine, IL-10, antagonizes certain effects of IL-1. We investigated the effect of IL-10 on IL-1␤-induced inhibition of LTP and glutamate release. The evidence presented indicates that IL-1␤ stimulates the stress-activated protein kinase, c-Jun-activated protein kinase (JNK), and IL-1 receptor-associated kinase, which may explain its inhibitory effect on release and LTP, and that IL-10 reversed the IL-1␤-induced stimulation of JNK activity and inhibition of release and LTP. We observed that IL-10 abrogated the stimulatory effect of IL-1␤ on superoxide dismutase activity and reactive oxygen species production, whereas the H 2 O 2 -induced inhibition of LTP was also blocked by IL-10. We present evidence that suggests that the action of IL-10 may be mediated by its ability to induce shedding of the IL-1 type I receptor.

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“…Furthermore, IL-1 family cytokines consist of six principle, related family members, i.e., three receptor ligands (IL-1α, IL-1β and IL-1 receptor antagonist (IL-1Ra)), two receptor subtypes (IL-1RI and IL-1RII) and an accessory protein (IL-1AcP) (Dinarello, 1996). These IL-1 family inflammatory mediators show cell-specific patterns of production, expression and release since ligands are made principally by glia (and some neurons) while astrocytes and neurons express the signal transducing IL-1 receptor, IL-1RI (Ban et al, 1991(Ban et al, , 1993Fontana et al, 1982;Giulian et al, 1986;Lechan et al, 1990). In addition, neurons (and glia) can be differentially distributed between and within various brain regions (Dombrowski et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

Optimization of multiplexed bead-based cytokine immunoassays for rat serum and brain tissue

Hulse

Kunkler

Fedynyshyn

et al. 2004

Journal of Neuroscience Methods

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The ability to simultaneously quantify multiple signaling molecule protein levels from microscopic neural tissue samples would be of great benefit to deciphering how they affect brain function. This follows from evidence that indicates signaling molecules can be pleiotropic and can have complex interactive behavior that is regionally and cellularly heterogeneous. Multiplexed examination of tissue proteins has been exceedingly difficult because of the absence of available techniques. This void now has been removed by the commercial availability of bead-based immunoassays for targeted proteins that allow analyses of up to 100 (6-150 kDa) proteins from as little as 12 μl. Thus far used only for sera (human and mouse) and culture media, we demonstrate here that sensitive (as low as 2 pg/ml), wide-ranging (up to 2-32 000 pg/ml), accurate (8% intra-assay covariance) and reliable (4-7% inter-assay covariance) measurements can be made of nine exemplary cytokines (e.g., IL-1α, IL-1β, IL-2, IL-4, IL-6, IL-10, GM-CSF, IFN-γ, TNF-α) simultaneously not only from rat serum but, for the first time, also brain tissue. Furthermore, we describe animal handling procedures that minimize stress as determined by serum glucocorticoid levels since they can influence cytokine expression.

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Immunoreactive interleukin-1β localization in the rat forebrain

Cited by 347 publications

References 32 publications

A Molecular Platform in Neurons Regulates Inflammation after Spinal Cord Injury

A Molecular Platform in Neurons Regulates Inflammation after Spinal Cord Injury

The Anti-inflammatory Cytokine, Interleukin (IL)-10, Blocks the Inhibitory Effect of IL-1β on Long Term Potentiation

Optimization of multiplexed bead-based cytokine immunoassays for rat serum and brain tissue

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