Interleukin-4 and interleukin-10 regulate IL1-? induced mouse primary astrocyte activation: A comparative study

Pousset, F.; Cremona, Sandrine; Dantzer, Robert; Kelley, Kevin W.; Parnet, Patricia

doi:10.1002/(sici)1098-1136(199903)26:1<12::aid-glia2>3.0.co;2-s

Cited by 69 publications

(46 citation statements)

References 52 publications

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“…It remains to be established whether, in the latter two studies, IL-10 inhibited production of IL-1 as it does in macrophages (24) or whether it antagonizes the effect of IL-1. In this context, it is significant that IL-10 (at the same concentration used in the present study) has been shown to inhibit the IL-1␤-induced increase in IL-6 production in astrocytes (53) and RANTES (regulated on activation normal T cell expressed and secreted) mRNA expression in microglia (54).…”

Section: Il-10 Antagonizes Il-1␤ Effect In Hippocampusmentioning

confidence: 57%

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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Section: Il-10 Antagonizes Il-1␤ Effect In Hippocampusmentioning

confidence: 57%

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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“…Glucocorticoids also interact with brain cells, e.g., dexamethasone inhibits the enhanced MHC class II antigen expression on microglial cells after axotomy [17]. In addition, it has been reported that cortisone inhibits IL-1-induced IL-6 production in astrocytes [27], and inhibits GM-CSF mRNA accumulation in IL-1-treated astrocytoma cells. [23].…”

Section: Discussionmentioning

confidence: 99%

Enhancement of antimicrobial effects by glucocorticoids

Türck

Oberdörfer

Vogel

et al. 2003

Med Microbiol Immunol

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In the past few years a body of evidence has accumulated showing that stimulation of human astrocytes and microvascular endothelial cells with IFN-gamma induces a potent antibacterial and anti-parasitic effect. We have found that the IFN-gamma-mediated activation of the tryptophan-degrading enzyme indoleamine 2,3-dioxygenase (IDO) is, at least in part, responsible for this antimicrobial activity. Glucocorticoids are frequently used in inflammatory central nervous system diseases to reduce the inflammatory reaction and cerebral edema. Since in many inflammatory conditions infection is either a primary or secondary factor, steroids are administered, in these circumstances, during infection. We investigated whether steroids could affect the antimicrobial effect of IFN-gamma-induced IDO activation. We found that hydrocortisone and dexamethasone enhance IFN-gamma-mediated IDO activity in both human astrocytoma cells and native human astrocytes. Furthermore, we found that the amounts of IDO mRNA and of IDO protein are enhanced in cells treated with IFN-gamma and glucocorticoids. In addition, we were able to demonstrate that both steroids enhance the IFN-gamma-mediated antimicrobial activity against Toxoplasma gondii, Staphylococcus aureus and group B streptococci. The enhanced antimicrobial effect of IFN-gamma in the presence of glucocorticoids is due to the enhancement of the IDO-mediated tryptophan degradation, demonstrated by the complete abrogation of this antimicrobial effect by tryptophan resupplementation. These data show that glucocorticoids, which were often used to inhibit proinflammatory processes, do not decrease IDO-mediated antimicrobial effects. In contrast, high doses of steroids were able to enhance the IFN-gamma-induced antimicrobial activity.

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“…Primary cultures of mouse neonatal astrocytes were generated (ϳ99% positivity for GFAP) after purification of astrocytes as described. 30 Primary cultures of mixed glia were prepared from newborn mice as described. 31 Pure microglia were magnetically isolated from primary cultures of mixed glia using CD11b microbeads from Miltenyi Biotech (Bergisch Gladbach, Germany), according to the manufacturer's instructions.…”

Section: Expression Of Lactadherin In Cultured Cells and Supernatantsmentioning

confidence: 99%

Evidence of a Role for Lactadherin in Alzheimer's Disease

Boddaert

Kinugawa²,

Lambert³

et al. 2007

The American Journal of Pathology

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Lactadherin is a secreted extracellular matrix protein expressed in phagocytes and contributes to the removal of apoptotic cells. We examined lactadherin expression in brain sections of patients with or without Alzheimer's disease and studied its role in the phagocytosis of amyloid ␤-peptide (A␤). Cells involved in Alzheimer's disease, including vascular smooth muscle cells, astrocytes, and microglia, showed a time-related increase in lactadherin production in culture. Quantitative analysis of the level of lactadherin showed a 35% reduction in lactadherin mRNA expression in the brains of patients with Alzheimer's disease (n ‫؍‬ 52) compared with age-matched controls (n ‫؍‬ 58; P ‫؍‬ 0.003). Interestingly, lactadherin protein was detected in the brains of patients with Alzheimer's disease and controls, with low expression in areas rich in senile plaques and marked expression in areas without A␤ deposition. Using surface plasmon resonance, we observed a direct pro-

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Interleukin-4 and interleukin-10 regulate IL1-? induced mouse primary astrocyte activation: A comparative study

Cited by 69 publications

References 52 publications

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

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

Enhancement of antimicrobial effects by glucocorticoids

Evidence of a Role for Lactadherin in Alzheimer's Disease

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