Localization of TNFα and IL-1a immunoreactivities in striatal neurons after surgical injury to the hippocampus

Tchélingérian, Jean‐Léon; Quinonero, Jérôme; Booss, John; Jacque, C.

doi:10.1016/0896-6273(93)90312-f

Cited by 175 publications

(88 citation statements)

References 41 publications

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“…IL-1␣ and TNF␣ are synthesized by those neurons where the ir is detected, as judged by detection of their mRNA in situ (eg Figure 1i). 35 This suggests that the cytokines remain cell-bound rather than diffuse to activate distant cells.…”

Section: Centrally Elicited Cytokine Signalingmentioning

confidence: 99%

“…IL-1␣ and TNF␣ are induced in neurons after a surgical lesion to the right hemisphere and their expression propagates to various regions of the brain in a spatiotemporal pattern. 35 Twenty-four hours after the lesion, intense IL-1␣ and TNF␣ ir appears in the striatum in the right hemisphere, ie, at a distance from the lesion (Figure 1a and b) but, not in the hippocampus itself. IL-1R density decreases, IL-1Ra mRNA level strongly increases and IL-1 (␣ and ␤) mRNA levels remain unchanged around the lesion.…”

Section: Centrally Elicited Cytokine Signalingmentioning

confidence: 99%

“…35 However, glial cells may also initiate cytokine signal propagation after some central perturbations. For example, A␤ [25][26][27][28][29][30][31][32][33][34][35] injected into amygdala increases IL-1␤ ir first in microglia of the amygdala and later in distant hippocampal neurons. 41 This suggests that cell types propagating cytokine signals vary with the nature of the perturbation eliciting the signal.…”

Section: Centrally Elicited Cytokine Signalingmentioning

confidence: 99%

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Cytokine signals propagate through the brain

et al. 2000

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Interleukin-1 (IL-1) and tumor necrosis factor alpha (TNF␣) are proinflammatory cytokines that are constitutively expressed in healthy, adult brain where they mediate normal neural functions such as sleep. They are neuromodulators expressed by and acting on neurons and glia. IL-1 and TNF␣ expression is upregulated in several important diseases/disorders. Upregulation of IL-1 and/or TNF␣ expression, elicited centrally or systemically, propagates through brain parenchyma following specific spatio-temporal patterns. We propose that cytokine signals propagate along neuronal projections and extracellular diffusion pathways by molecular cascades that need to be further elucidated. This elucidation is a prerequisite for better understanding of reciprocal interactions between nervous, endocrine and immune systems. Molecular Psychiatry (2000) 5, 604-615.

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Section: Centrally Elicited Cytokine Signalingmentioning

confidence: 99%

Section: Centrally Elicited Cytokine Signalingmentioning

confidence: 99%

Section: Centrally Elicited Cytokine Signalingmentioning

confidence: 99%

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Cytokine signals propagate through the brain

et al. 2000

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“…E-mail: Shen.Yong@igate.abbott.com. 1 The abbreviations used are: TNF, tumor necrosis factor; TNFR, TNF receptor; ASO, antisense oligonucleotide; LDH, lactate dehydrogenase; RA, retinoic acid; PCR, polymerase chain reaction; hTNF, human TNF; A␤, ␤-amyloid peptide; SO, sense oligonucleotide; RT, reverse transcriptase. cysteine for 2 h followed by incubation with [ 35 S]methionine and [ 35 S]cysteine (50 Ci/ml, DuPont NEN) in methionine-and cysteinefree medium at 37°C.…”

Section: Methodsmentioning

confidence: 99%

“…Tumor necrosis factor-␣ (TNF-␣), 1 an inflammatory mediator, is recently reported to be up-regulated following brain trauma (1,2) and ischemic injury (3,4), and in multiple sclerosis (5,6), Parkinson's disease (7), and Alzheimer's disease (8). Studies have shown that TNF-␣ can elicit either a trophic or toxic effect, which is dependent on the target cell type.…”

Section: Recent Evidence Indicates That Tumor Necrosis Factor-␣ (Tnf-mentioning

confidence: 99%

Inhibition of p75 Tumor Necrosis Factor Receptor by Antisense Oligonucleotides Increases Hypoxic Injury and β-Amyloid Toxicity in Human Neuronal Cell Line

Shen

Shiosaki

1997

Journal of Biological Chemistry

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Recent evidence indicates that tumor necrosis factor-␣ (TNF-␣) is up-regulated following brain injury andin neurodegenerative disorders such as stroke, multiple sclerosis, Parkinson's disease, and Alzheimer's disease. TNF-␣ elicits its biological effects through two distinct TNF receptor (TNFR) subtypes: p55 TNFR (TNFR1) and p75 TNFR (TNFR2). Studies have demonstrated that the p55 TNFR contributes to cell death, whereas the role of the p75 TNFR in neuronal viability is unclear. To better understand the role of p75 TNFR, we treated human neuronal SH-SY5Y cells with phosphorothioate-modified antisense oligonucleotides (ASO) for p75 TNFR and established that ASO inhibited p75 TNFR expression. Treatment of SH-SY5Y cells with ASO alone did not affect cell viability, whereas treatment with both ASO and human TNF-␣ significantly increased cell death relative to treatment with TNF-␣ alone. Moreover, addition of ASO significantly increased the level of cell injury observed following hypoxic conditions or exposure of ␤-amyloid peptide. These results indicate that inhibition of p75 TNFR using ASO increases the vulnerability of neurotypic cells to insults and suggest that the p75 TNFR may not be required for normal neuronal cell viability but rather plays a protective role following injury.Tumor necrosis factor-␣ (TNF-␣), 1 an inflammatory mediator, is recently reported to be up-regulated following brain trauma (1, 2) and ischemic injury (3, 4), and in multiple sclerosis (5, 6), Parkinson's disease (7), and Alzheimer's disease (8). Studies have shown that TNF-␣ can elicit either a trophic or toxic effect, which is dependent on the target cell type. For example, TNF-␣ is toxic to human oligodendrocytes (9) and neuronal cells (10, 11), but it is trophic to rat hippocampal neurons (12). Since TNF-␣ elicits its biological effects through activation of two distinct receptors, p55 TNFR and p75 TNFR, both of which have been cloned (13-15), we hypothesized that the distinct TNF receptor subtypes might contribute to the multiple biological functions of TNF-␣. Reports indicate that the p55 TNFR may contribute to cell death (16), whereas the role of the p75 TNFR in neuronal cell function is not clear. Here we show that inhibition of p75 TNFR by antisense oligonucleotides (ASO) increased the magnitude of neuronal cell death induced by TNF-␣, hypoxic injury or ␤-amyloid peptide (A␤) as measured by lactate dehydrogenase (LDH) release. This novel finding provides evidence that the p75 TNFR might play a protective role following neuronal insult. EXPERIMENTAL PROCEDURESCell Cultures-Human neuronal-like cells, SH-SY5Y, were cultured in a 1:1 ratio of minimum Eagle's medium/F-12 medium, 15% fetal calf serum (Life Technologies, Inc.), and 10 M retinoic acid (RA, Sigma). The cells were seeded at 25,000 cells/well in a 24-well plate for cytotoxicity assays or 3 ϫ 10 6 cells in Petri dishes for radioimmunoprecipitation study. The medium was replaced every 3 days. Treatments were given to the cells in serum-free medium with 1:100 N2-supplement (Li...

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Induction of cytokine transcripts in the central nervous system and pituitary following peripheral administration of endotoxin to mice

et al. 1997

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The regional distribution and inducibility of cytokines in the normal brain is still a matter of controversy. As an attempt to clarify this issue, we studied the constitutive and induced expression of interleukin (IL)-1beta, IL-6, tumor necrosis factor (TNF)-alpha, and interferon (IFN)-gamma mRNAs in the brain, pituitary, and spleen of mice using qualitative and semiquantitative reverse-transcription polymerase chain reaction. The contribution of nonbrain cells to the cytokine transcripts detected was considered. With the exception of IFN-gamma mRNA, transcripts for the other cytokines were found to be constitutively present in the brain. Following i.p. injection of lipopolysaccharide (LPS) at a dose below those described to disrupt the blood-brain barrier (BBB), cytokine mRNA expression was increased in the spleen, the pituitary, and the brain. In the brain, the onset of transcription varied from 45 min (IL-1beta, TNF-alpha) to 4 hr (IFN-gamma), and the peak of mRNA accumulation was observed at different times depending on the cytokine and the brain region studied. IL-1 and IL-6 were highly expressed in the hypothalamus and hippocampus, while TNF-alpha expression was more marked in the thalamus-striatum. The cortex was the region in which cytokines were less inducible. The inducible expression of cytokine mRNAs in the brain was paralleled by stimulation of the hypothalamus-pituitary-adrenal axis. These results show the capacity of brain cells to synthesize different cytokine mRNAs in vivo and define the kinetics of their expression in several brain areas and in the periphery in parallel to the activation of a neuroendocrine pathway by endotoxin.

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Localization of TNFα and IL-1a immunoreactivities in striatal neurons after surgical injury to the hippocampus

Cited by 175 publications

References 41 publications

Cytokine signals propagate through the brain

Cytokine signals propagate through the brain

Inhibition of p75 Tumor Necrosis Factor Receptor by Antisense Oligonucleotides Increases Hypoxic Injury and β-Amyloid Toxicity in Human Neuronal Cell Line

Induction of cytokine transcripts in the central nervous system and pituitary following peripheral administration of endotoxin to mice

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