The Brain innate immune response in neuroprotection and repair

Abstract

Event Abstract Back to Event The Brain innate immune response in neuroprotection and repair Serge Rivest1* 1 Laval University, Department of Anatomy and Physiology, Canada Although cytokines can be produced by and act on most cells of the central nervous system (CNS), microglia are thought to be the main cell type of the innate immune system in the brain. Microglia are present throughout the CNS; there are regions that are more populated than others and the white matter generally contains less microglia than the grey matter. They are highly ramified cells and their processes are very active and plastic even during normal conditions. Similar to macrophages, microglia express Toll-like receptors (TLRs), respond to TLR ligands and produce inflammatory mediators. Of interest is the fact that these immune cells can be activated during systemic infections without the integrity of the blood–brain barrier (BBB) being compromised. There are regions in the brain that have no BBB and the response to circulating pathogens at these sites is similar to that in most systemic organs. The circumventricular organs (CVOs) are strategically positioned to sensor pathogen-associated molecular patterns (PAMPs) in the blood. Rapid innate immune responses to systemic infection are initiated at these regions, which are followed by a progressing activation of resident microglia in the brain parenchyma. The characterization of a rapid brain response to systemic infections challenged the concept of the immune-privileged status of the CNS, which was originally believed to be essentially devoid of immune cells and therefore immune responses. Activation of innate immune signalling pathways in resident microglia not only occurs in response to infectious organisms, but also during brain injury and chronic disease. In addition, a marked recruitment, proliferation and activation of microglia precursors is detected in affected regions of the brain. It is possible that under certain conditions, the recruitment and activation of microglia precursors and the activation of resident microglia should be suppressed to avoid extended damage to the brain tissue, whereas under other conditions, restricting the innate immune response mediated by these cells may impair regenerative processes and immunity against invading pathogens and endogenously produced toxic proteins. In addition, the reduced ability of microglia to clear toxic proteins may actually be part of the pathogenic mechanisms involved in neurodegenerative diseases, the best example being the extracellular accumulation of amyloid beta in the brain of patients with Alzheimer's disease. This talk will discuss some of the molecular details of the innate immune response in the brain and how it can be directed towards neuroprotection and repair. Conference: 11th Meeting of the Portuguese Society for Neuroscience, Braga, Portugal, 4 Jun - 6 Jun, 2009. Presentation Type: Oral Presentation Topic: Plenary lectures Citation: Rivest S (2009). The Brain innate immune response in neuroprotection and repair. Front. Neurosci. Conference Abstract: 11th Meeting of the Portuguese Society for Neuroscience. doi: 10.3389/conf.neuro.01.2009.11.001 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 04 Aug 2009; Published Online: 04 Aug 2009. * Correspondence: Serge Rivest, Laval University, Department of Anatomy and Physiology, Beauport, Qc G1J 2G3, Canada, serge.rivest@crchul.ulaval.ca Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Serge Rivest Google Serge Rivest Google Scholar Serge Rivest PubMed Serge Rivest Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.