Adhesion to fibronectin regulates interleukin-1 beta expression in microglial cells

Lauren Summers, Cay Kielty, Emmanuel Pinteaux

    Research output: Contribution to journalArticlepeer-review


    The extracellular matrix (ECM) of the central nervous system (CNS) is rapidly degraded following acute brain injury, leading to inflammation and neuronal death. Under these conditions, the pro-inflammatory cytokine interleukin-1β (IL-1β) is primarily produced by microglial cells and is a key mediator of neuroinflammation, but whether the ECM regulates microglial IL-1 synthesis after CNS injury remains unknown. This study aimed to investigate whether cell attachment to ECM molecules modulated IL-1β production in activated microglia in vitro. We found adhesion to fibronectin, fibrillin-1 and laminin promoted microglial cell adhesion and spreading, potentiated by bacterial lipopolysaccharide (LPS) treatment. Adhesion to fibronectin (but not fibrillin-1 or laminin) regulated IL-1β expression via a cell density-dependent mechanism, whereby fibronectin-induced cell proliferation resulted in less IL-1β being produced. These data suggest an important regulatory mechanism of IL-1 production, associated with microglial migration and proliferation, driven by ECM degradation and/or synthesis in an injured brain. © 2009 Elsevier Inc. All rights reserved.
    Original languageEnglish
    Pages (from-to)148-155
    Number of pages7
    JournalMolecular and Cellular Neuroscience
    Issue number2
    Publication statusPublished - 1 Jun 2009


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