Localization of interleukin 6 mRNA and interleukin 6 receptor mRNA in rat brain

Schöbitz, Bernd; Voorhuis, Dorothy A.M.; Kloet, E. Ronald de

doi:10.1016/0304-3940(92)90046-a

Cited by 187 publications

(67 citation statements)

References 9 publications

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“…It has also been reported that IL-1 receptors antagonist ameliorates learning and . Due to a high density cytokines receptors, hippocampus has been considered to be very vulnerable to inflammation 27 . Using animal models, it has been indicated that administration of cytokines or other immune system stimuli including LPS deteriorate hippocampus-dependent learning and memory process 24 .…”

Section: Discussionmentioning

confidence: 99%

Lipopolysaccharide-induced memory impairment in rats is preventable using 7-nitroindazole

Anaeigoudari

Shafei

Soukhtanloo

et al. 2015

Arq. Neuro-Psiquiatr.

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Inflammation and oxidative stress have important roles in memory impairment. The effect of 7-nitroindazole (7NI) on lipopolysaccharide (LPS)-induced memory impairment was investigated. Rats were used, divided into four groups that were treated as follows: (1) control (saline); (2) LPS; (3) 7NI-LPS; and (4) 7NI before passive avoidance (PA). In the LPS group, the latency for entering the dark compartment was shorter than in the controls (p < 0.01 and p < 0.001); while in the 7NI-LPS group, it was longer than in the LPS group (p < 0.01 and p < 0.001). Malondialdehyde (MDA) and nitric oxide (NO) metabolite concentrations in the brain tissues of the LPS group were higher than in the controls (p < 0.001 and p < 0.05); while in the 7NI-LPS group, they were lower than in the LPS group (p < 0.001 and p < 0.05, respectively). The thiol content in the brain of the LPS group was lower than in the controls (p < 0.001); while in the 7NI-LPS group, it was higher than in the LPS group (p < 0.001). It is suggested that brain tissue oxidative damage and NO elevation have a role in the deleterious effects of LPS on memory retention that are preventable using 7NI.

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Section: Discussionmentioning

confidence: 99%

Lipopolysaccharide-induced memory impairment in rats is preventable using 7-nitroindazole

Anaeigoudari

Shafei

Soukhtanloo

et al. 2015

Arq. Neuro-Psiquiatr.

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“…In the CNS, IL-6 is found in neurons, glial cells, and macrophages (Schobitz et al, 1992;Gadient and Otten, 1995), and, although expression levels are low under normal conditions, increases occur after brain injury, inflammation, and neuronal disease (Strauss et al, 1992;Tarkowski et al, 1995). Proposed roles for IL-6 include glia proliferation, neuronal survival and differentiation, and pro-inflammatory activities (Hama et al, 1991;Hirota et al, 1996;Klein et al, 1997;Marz et al, 1997;Loddick et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

The Cytokine Interleukin-6 Is Sufficient But Not Necessary to Mimic the Peripheral Conditioning Lesion Effect on Axonal Growth

Cao¹,

Gao²,

Bryson³

et al. 2006

J. Neurosci.

174

147

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Lesioning the peripheral branch of a dorsal root ganglion (DRG) neuron before injury of the central branch of the same neuron enables spontaneous regeneration of these spinal axons. This effect is cAMP and transcription dependent. Here, we show that the cytokine interleukin-6 (IL-6) is upregulated in DRG neurons after either a conditioning lesion or treatment with dibutyryl-cAMP. In culture, IL-6 allows neurons to grow in the presence of inhibitors of regeneration present in myelin. Importantly, intrathecal delivery of IL-6 to DRG neurons blocks inhibition by myelin both in vitro and in vivo, effectively mimicking the conditioning lesion. Blocking IL-6 signaling has no effect on the ability of cAMP to overcome myelin inhibitors. Consistent with this, IL-6-deficient mice respond to a conditioning lesion as effectively as wild-type mice. We conclude that IL-6 can mimic both the cAMP effect and the conditioning lesion effect but is not an essential component of either response.

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“…A possible role of centrally produced IL-6 might be to support the local immune reaction by repressing neurotoxic inflammatory processes, increasing antibody secretion, inducing gliosis, and stimulating cells that form the blood-brain barrier (astrocytes and microglial and endothelial cells) to promote leukocyte infiltration (Schöbitz et al, 1994). on the other hand, the presence of IL-6 in the brain of unstimulated animals is still controversial; although some investigators have detected a positive signal for IL-6 mRNA only after stimulation (Murphy et al, 1995), others have reported a constitutive expression of the transcript in several brain areas (Schöbitz et al, 1992(Schöbitz et al, , 1993Gadient and Otten, 1994). Although it may suggest additional functions, the role of IL-6 as an alarm signal and the adverse effects that may occur after a prolonged exposure are two arguments against the possibility that IL-6 is secreted throughout the brain at elevated levels under basal conditions.…”

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confidence: 99%

“…Basal expression of IL-6R mRNA was found in several regions of the brain, particularly in white matter (Schöbitz et al, 1992(Schöbitz et al, , 1993Otten, 1993, 1994). However, the fact that IL-6R mRNA or its corresponding protein has not been identified in the sensorial CVOs constitutes a major obstacle to support for the assumption that these structures are sites of action for the circulating proinflammatory cytokine.…”

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confidence: 99%

Regulation of the Genes Encoding Interleukin‐6, Its Receptor, and gp130 in the Rat Brain in Response to the Immune Activator Lipopolysaccharide and the Proinflammatory Cytokine Interleukin‐1β

Vallières

Rivest

1997

Journal of Neurochemistry

289

181

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Interleukin-6 (IL-6) is a pleiotropic cytokirie believed to play key roles in the neuroimmune interactions. This molecule may act on the nervous system by interacting with its specific receptor subunit (IL-6R) and the signal transducer gp130. The purposes of the present study were to describe the central distribution of IL-6, IL-6R, and gpl3O mRNAs under basal conditions and to verify the influence of the immune activator lipopolysaccharide (LPS) and the proinflammatory cytokine interleukm-1/3 (IL-1/3) on the expression of IL-6 and its related genes throughout the rat brain. Rats were killed at multiple times after intraperitoneal injection of the bacterial endotoxin and intravenous administration of the recombinant rat IL-1/3 (rrlL-1ß), and their brains were cut into 30-~zmcoronal sections from the olfactory bulb to the end of the medulla. Each transcript was localized by in situ hybridization histochemistry using 35S-labeled rat riboprobes. The results show that IL-6 mRNA was undetectable in the brain under basal conditions and following the injection of rrlL-1/3. Injection of LPS rapidly stimulated transcription of this gene in the choroid plexus and the sensorial circumventricular organs (CVOs), including the organum vasculosum Iaminae terminalis (OVLT), subfornical organ, median eminence, and area postrema. Conversely, IL-6R and gpl3O mRNAs were heterogeneously distributed throughout the brain under basal conditions. The injection of LPS stimulated the biosynthesis of IL-6R in the CVOs, medial preoptic area, bed nucleus stria terminalis, central nucleus of the amygdala, hippocampus, hypothalamic paraventricular nucleus, cerebral cortex, and blood vessels. Increased levels of IL-6R mRNA were also observed in the microvasculature following rrlL-1/3 injection. Finally, gp130 mRNA expression was increased in the OVLT and throughout the endothelium of brain capillaries of LPS-treated rats but remained unchanged after administration of rrIL-1/3. These results demonstrate that expression of the genes encoding IL-6, IL-6R, and gpl3O can be up-regulated in selective regions of the brain in response to the bacterial endotoxin LPS and the proinflammatory cytokine IL-1/3 (only for IL-6R expression). This fine genetic regulation might be of great importance in the neuroimmune interplay and provides the evidence that sensorial CVOs and microvasculature are in a privileged position to mediate the action of IL-6 of central and/or systemic origin in the brain of immune-challenged animals. Key Words: Brain-c-fosCircumventricular organs-Cytokines-gpl 30-Immune response-In situ hybridization -Interleukin-1 -Interleukin-6-Lipopolysaccharide-mRNA-Neuroimmunology-Rat-Receptor.

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Localization of interleukin 6 mRNA and interleukin 6 receptor mRNA in rat brain

Cited by 187 publications

References 9 publications

Lipopolysaccharide-induced memory impairment in rats is preventable using 7-nitroindazole

Lipopolysaccharide-induced memory impairment in rats is preventable using 7-nitroindazole

The Cytokine Interleukin-6 Is Sufficient But Not Necessary to Mimic the Peripheral Conditioning Lesion Effect on Axonal Growth

Regulation of the Genes Encoding Interleukin‐6, Its Receptor, and gp130 in the Rat Brain in Response to the Immune Activator Lipopolysaccharide and the Proinflammatory Cytokine Interleukin‐1β

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