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Protective effects of an anti-inflammatory cytokine, interleukin-4, on motoneuron toxicity induced by activated microglia.

Protective effects of an anti-inflammatory cytokine, interleukin-4, on motoneuron toxicity induced by activated microglia. Research Abstract Details 

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  • Protective effects of an anti-inflammatory cytokine, interleukin-4, on motoneuron toxicity induced by activated microglia. Abstract Text:

    weihua zhaoWeihua Zhao,wenjie xieWenjie Xie,qin xiaoQin Xiao,david r beersDavid R Beers,stanley h appelStanley H Appel,

    Microglia-mediated cytotoxicity has been implicated in models of neurodegenerative diseases, such as amyotrophic lateral sclerosis, Parkinson's disease and Alzheimer's disease, but few studies have documented how neuroprotective signals might mitigate such cytotoxicity. To explore the neuroprotective mechanism of anti-inflammatory cytokines, we applied interleukin-4 (IL-4) to primary microglial cultures activated by lipopolysaccharide as well as to activated microglia cocultured with primary motoneurons. lipopolysaccharide increased nitric oxide and superoxide (O(2) (.-)) and decreased insulin-like growth factor-1 (IGF-1) release from microglial cultures, and induced motoneuron injury in microglia-motoneuron cocultures. However, lipopolysaccharide had minimal effects on isolated motoneuron cultures. IL-4 interaction with microglial IL-4 receptors suppressed and nitric oxide release, and lessened lipopolysaccharide-induced microglia-mediated motoneuron injury. The extent of nitric oxide suppression correlated directly with the extent of motoneuron survival. Although IL-4 enhanced release of free IGF-1 from microglia in the absence of lipopolysaccharide, it did not enhance free IGF-1 release in the presence of lipopolysaccharide. These data suggest that IL-4 may provide a significant immunomodulatory signal which can protect against microglia-mediated neurotoxicity by suppressing the production and release of free radicals.

    Protective effects of an anti-inflammatory cytokine, interleukin-4, on motoneuron toxicity induced by activated microglia. Publishing Authors By Initials

    w zhaoW Zhao,w xieW Xie,q xiaoQ Xiao,dr beersDR Beers,sh appelSH Appel,

    For similar inorganic chemicals: electrolytes: ions: anions: oxides: peroxides: superoxides research abstracts see: inorganic chemicals: electrolytes: ions: anions: oxides: peroxides: superoxides research

    PUBMED ID PMID:

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    Protective effects of an anti-inflammatory cytokine, interleukin-4, on motoneuron toxicity induced by activated microglia. Journal Published:

    PUBLICATION TYPE: Research Support, Non-U.S. Gov

    Journal: Journal of neurochemistry

    VOLUME: 99

    Page Numbers: 1176-87

    Journal Abbreviation: J. Neurochem.

    ISSN: 0022-3042

    DAY: 2

    MONTH: 10

    YEAR: 2006

    Protective effects of an anti-inflammatory cytokine, interleukin-4, on motoneuron toxicity induced by activated microglia. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 2985190

    Protective effects of an anti-inflammatory cytokine, interleukin-4, on motoneuron toxicity induced by activated microglia. Keywords Mesh Terms:

    KEYWORDS: Superoxides

    MESH TERMS: metabolism

    Chemical & Substance for Abstract: Protective effects of an anti-inflammatory cytokine, interleukin-4, on motoneuron toxicity induced by activated microglia. Information

    Substance Name: Insulin-Like Growth Factor I

    Registry Number: 67763-96-6

    Grant and Affiliation Information for Protective effects of an anti-inflammatory cytokine, interleukin-4, on motoneuron toxicity induced by activated microglia.

    AFFILIATION: Department of Neurology, Methodist Neurological Institute, The Methodist Hospital, Houston, Texas 77030, USA.

    Country: England

    England Research PublicationEngland Research Publication

    AGENCY: United States NINDS

    GRANT: 1R01NS048950-01

    ACRONYM: NS

    MEDLINETA: J Neurochem

    REFSOURCE:

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    ACCESSION NUMBER:

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