Interleukin-1 binding sites on astrocytes

Ban, Eunmi; Sarliève, Louis L.; Haour, F.

doi:10.1016/0306-4522(93)90421-b

Cited by 94 publications

(46 citation statements)

References 43 publications

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“…Several lines of evidence support a role for inflammatory cytokines as mediators of astrogliosis. Receptors for IFN-␥, IL-1, IL-6, IL-7, IL-10, granulocyte macrophage colony stimulating factor (GM-CFS), and macrophage colony stimulating factor (M-CSF) have been demonstrated on astrocytes (Rubio and de Felipe, 1991;Ban et al, 1993;Sawada et al, 1993;Mizuno et al, 1994;Tada et al, 1994;St. Pierre et al, 1996).…”

Section: Discussionmentioning

confidence: 99%

Astrogliosis in the Neonatal and Adult Murine Brain Post-Trauma: Elevation of Inflammatory Cytokines and the Lack of Requirement for Endogenous Interferon-γ

et al. 1997

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The relevance of astrogliosis remains controversial, especially with respect to the beneficial or detrimental influence of reactive astrocytes on CNS recovery. This dichotomy can be resolved if the mediators of astrogliosis are identified. We have measured the levels of transcripts encoding inflammatory cytokines in injury systems in which the presence or absence of astrogliosis could be produced selectively. A stab injury to the adult mouse brain using a piece of nitrocellulose (NC) membrane elicited a prompt and marked increase in levels of transcripts for interleukin (IL)-1α, IL-1β, and tumor necrosis factor (TNF)-α, which are considered to be microglia/macrophage cytokines. The elevations preceded, or occurred concomitantly with, the rise in glial fibrillary acidic protein mRNA, an early manifestation of astrogliosis. In neonatal mice, IL-1 and TNF-α mRNA were elevated to a greater extent by an NC-implant injury, which produced astrogliosis, than after an NC-stab, with minimal astrogliosis. We determined whether endogenous interferon (IFN)-γ could be responsible for the observed increases in IL-1 and TNF-α, because IFN-γ is a potent microglia/macrophage activator, and because its exogenous administration to rodents enhanced astrogliosis after adult or neonatal insults. A lack of requirement for endogenous IFN-γ was demonstrated by three lines of evidence. First, no increase in IFN-γ transcripts could be found at injury. Second, the administration of a neutralizing antibody to IFN-γ did not attenuate astrogliosis. Third, in IFN-γ knockout adult mice, astrogliosis and increases in levels of IL-1α and TNF-α were induced rapidly by injury. The marked elevation of inflammatory cytokines is discussed in the context of astrogliosis and general CNS recovery.

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Section: Discussionmentioning

confidence: 99%

Astrogliosis in the Neonatal and Adult Murine Brain Post-Trauma: Elevation of Inflammatory Cytokines and the Lack of Requirement for Endogenous Interferon-γ

et al. 1997

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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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“…IL-1 increases microglial proliferation in mixed astrocyte-microglial cell cultures, but has no effect on isolated microglia (Ganter et al 1992). In addition, iodinated IL-1a binds specifically to astrocytes, but not to microglial cells (Ban et al 1993), suggesting that microglial cells may not express IL-1 receptors. In contrast, recent studies have reported that IL-1 up-regulates the expression of Mac-1 and CD4 (Yu et al 1998), and induces the production of macrophage inflammatory protein (MIP)-1a and b (McManus et al 1998) in microglia, suggesting that these cells are targets for IL-1b.…”

mentioning

confidence: 96%

Expression of interleukin‐1 receptors and their role in interleukin‐1 actions in murine microglial cells

Pinteaux

Parker

Rothwell

et al. 2002

Journal of Neurochemistry

154

107

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Interleukin (IL)-1 is an important mediator of acute brain injury and inflammation, and has been implicated in chronic neurodegeneration. The main source of IL-1 in the CNS is microglial cells, which have also been suggested as targets for its action. However, no data exist demonstrating expression of IL-1 receptors [IL-1 type-I receptor (IL-1RI), IL-1 type-II receptor (IL-1RII) and IL-1 receptor accessory protein (IL-1RAcP)] on microglia. In the present study we investigated whether microglia express IL-1 receptors and whether they present target or modulatory properties for IL-1 actions. RT-PCR analysis demonstrated lower expression of IL-1RI and higher expression of IL-1RII mRNAs in mouse microglial cultures compared with mixed glial or pure astrocyte cultures. Bacterial lipopolysaccharide (LPS) caused increased expression of IL-1RI, IL-1RII and IL-1RAcP mRNAs, induced the release of IL-1b, IL-6 and prostaglandin-E 2 (PGE 2 ), and activated nuclear factor jB (NF-jB) and the mitogen-activated protein kinases (MAPKs) p38, and extracellular signal-regulated protein kinase (ERK1/2), but not c-Jun N-terminal kinase (JNK) in microglial cultures. In comparison, IL-1b induced the release of PGE 2 , IL-6 and activated NF-jB, p38, JNK and ERK1/2 in mixed glial cultures, but failed to induce any of these responses in microglial cell cultures. IL-1b also failed to affect LPS-primed microglial cells. Interestingly, a neutralizing antibody to IL-1RII significantly increased the concentration of IL-1b in the medium of LPS-treated microglia and exacerbated the IL-1b-induced IL-6 release in mixed glia, providing the first evidence that microglial IL-1RII regulates IL-1b actions by binding excess levels of this cytokine during brain inflammation. Keywords: interleukin 1 receptors, interleukin 1 signaling, microglial cells, mitogen-activated protein kinase, nuclear factor kappa B.

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Interleukin-1 binding sites on astrocytes

Cited by 94 publications

References 43 publications

Astrogliosis in the Neonatal and Adult Murine Brain Post-Trauma: Elevation of Inflammatory Cytokines and the Lack of Requirement for Endogenous Interferon-γ

Astrogliosis in the Neonatal and Adult Murine Brain Post-Trauma: Elevation of Inflammatory Cytokines and the Lack of Requirement for Endogenous Interferon-γ

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

Expression of interleukin‐1 receptors and their role in interleukin‐1 actions in murine microglial cells

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