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. 2012 Aug;1(2):195-211.

Interleukin-1β in Central Nervous System Injury and Repair

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Interleukin-1β in Central Nervous System Injury and Repair

Sandra J Hewett et al. Eur J Neurodegener Dis. 2012 Aug.

Abstract

Acute inflammation is a self-limiting, complex biological response mounted to combat pathogen invasion, to protect against tissue damage, and to promote tissue repair should it occur. However, unabated inflammation can be deleterious and contribute to injury and pathology. Interleukin-1β (IL-1β), a prototypical "pro-inflammatory" cytokine, is essential to cellular defense and tissue repair in nearly all tissues. With respect to brain, however, studies suggest that IL-1β has pleiotrophic effects. It acts as a neuromodulator in the healthy central nervous system (CNS), has been implicated in the pathogenic processes associated with a number of CNS maladies, but may also provide protection to the injured CNS. Here, we will review the physiological and pathophysiological functions of IL-1β in the central nervous system with regard to synaptic plasticity. With respect to disease, emphasis will be placed on stroke, epilepsy, Parkinson's disease and Alzheimer's disease where the ultimate injurious or reparative effects of IL-1β appear to depend on time, concentration and environmental milieu.

Keywords: IL-1; Injury; Interleukin 1; Neurodegeneration; Neuroinflammation; Neurological disease; Protection; Repair.

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References

    1. Albrecht PJ, Dahl JP, Stoltzfus OK, Levenson R, Levison SW. Ciliary neurotrophic factor activates spinal cord astrocytes, stimulating their production and release of fibroblast growth factor-2, to increase motor neuron survival. Exp Neurol. 2002;173:46–62. - PubMed
    1. Andre R, Moggs JG, Kimber I, Rothwell NJ, Pinteaux E. Gene regulation by IL-1beta independent of IL-1R1 in the mouse brain. Glia. 2006;53:477–83. - PubMed
    1. Andrei C, Margiocco P, Poggi A, Lotti LV, Torrisi MR, Rubartelli A. Phospholipases C and A2 control lysosome-mediated IL-1 beta secretion: Implications for inflammatory processes. Proc Natl Acad Sci U S A. 2004;101:9745–50. - PMC - PubMed
    1. Arend WP, Malyak M, Smith MF, Jr., Whisenand TD, Slack JL, et al. Binding of IL-1 alpha, IL-1 beta, and IL-1 receptor antagonist by soluble IL-1 receptors and levels of soluble IL-1 receptors in synovial fluids. J Immunol. 1994;153:4766–74. - PubMed
    1. Avital A, Goshen I, Kamsler A, Segal M, Iverfeldt K, et al. Impaired interleukin-1 signaling is associated with deficits in hippocampal memory processes and neural plasticity. Hippocampus. 2003;13:826–34. - PubMed