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      Danger signals in stroke and their role on microglia activation after ischemia

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          Abstract

          Ischemic stroke is a major cause of death. Besides the direct damage resulting from oxygen and glucose deprivation, sterile inflammation plays a pivotal role in increasing cellular death. Damaged-associated molecular patterns (DAMPs) are passively released from dying cells and activate the innate immune system. Thus, they take part in the direct and rapid activation of the inflammatory response after stroke onset. In this review the role of the most important DAMPs, high mobility group box 1, heat and cold shock proteins, purines, and peroxiredoxins, are addressed. Moreover, intracellular pathways activated by DAMPs in microglia are illuminated.

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          The inflammasomes: guardians of the body.

          Fabio Martinon, Annick Mayor, Jurg Tschopp (2009)
          The innate immune system relies on its capacity to rapidly detect invading pathogenic microbes as foreign and to eliminate them. The discovery of Toll-like receptors (TLRs) provided a class of membrane receptors that sense extracellular microbes and trigger antipathogen signaling cascades. More recently, intracellular microbial sensors have been identified, including NOD-like receptors (NLRs). Some of the NLRs also sense nonmicrobial danger signals and form large cytoplasmic complexes called inflammasomes that link the sensing of microbial products and metabolic stress to the proteolytic activation of the proinflammatory cytokines IL-1beta and IL-18. The NALP3 inflammasome has been associated with several autoinflammatory conditions including gout. Likewise, the NALP3 inflammasome is a crucial element in the adjuvant effect of aluminum and can direct a humoral adaptive immune response. In this review, we discuss the role of NLRs, and in particular the inflammasomes, in the recognition of microbial and danger components and the role they play in health and disease.
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            Microglial and macrophage polarization—new prospects for brain repair.

            Xiaoming Hu, Rehana Leak, Yejie Shi … (2015)
            The traditional view of the adult brain as a static organ has changed in the past three decades, with the emergence of evidence that it remains plastic and has some regenerative capacity after injury. In the injured brain, microglia and macrophages clear cellular debris and orchestrate neuronal restorative processes. However, activation of these cells can also hinder CNS repair and expand tissue damage. Polarization of macrophage populations toward different phenotypes at different stages of injury might account for this dual role. This Perspectives article highlights the specific roles of polarized microglial and macrophage populations in CNS repair after acute injury, and argues that therapeutic approaches targeting cerebral inflammation should shift from broad suppression of microglia and macrophages towards subtle adjustment of the balance between their phenotypes. Breakthroughs in the identification of regulatory molecules that control these phenotypic shifts could ultimately accelerate research towards curing brain disorders.
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              Microglia development and function.

              Debasis Nayak, Theodore L Roth, Dorian B McGavern (2014)
              Proper development and function of the mammalian central nervous system (CNS) depend critically on the activity of parenchymal sentinels referred to as microglia. Although microglia were first described as ramified brain-resident phagocytes, research conducted over the past century has expanded considerably upon this narrow view and ascribed many functions to these dynamic CNS inhabitants. Microglia are now considered among the most versatile cells in the body, possessing the capacity to morphologically and functionally adapt to their ever-changing surroundings. Even in a resting state, the processes of microglia are highly dynamic and perpetually scan the CNS. Microglia are in fact vital participants in CNS homeostasis, and dysregulation of these sentinels can give rise to neurological disease. In this review, we discuss the exciting developments in our understanding of microglial biology, from their developmental origin to their participation in CNS homeostasis and pathophysiological states such as neuropsychiatric disorders, neurodegeneration, sterile injury responses, and infectious diseases. We also delve into the world of microglial dynamics recently uncovered using real-time imaging techniques.
              Article 0 comments Cited 407 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Eileen Gülke
                Mathias Gelderblom
                Tim Magnus
                Journal
                Journal ID (nlm-ta): Ther Adv Neurol Disord
                Journal ID (iso-abbrev): Ther Adv Neurol Disord
                Journal ID (publisher-id): TAN
                Journal ID (hwp): sptan
                Title: Therapeutic Advances in Neurological Disorders
                Publisher: SAGE Publications (Sage UK: London, England )
                ISSN (Print): 1756-2856
                ISSN (Electronic): 1756-2864
                Publication date (Electronic): 22 May 2018
                Publication date Collection: 2018
                Volume: 11
                Electronic Location Identifier: 1756286418774254
                Affiliations
                [1-1756286418774254]Department of Neurology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany
                [2-1756286418774254]Department of Neurology, University Medical Center Hamburg-Eppendorf, Martinistraße 52, 20246 Hamburg, Germany
                [3-1756286418774254]Department of Neurology, University Medical Center Hamburg-Eppendorf, Martinistraße 52, 20246 Hamburg, Germany
                Author notes
                Article
                Publisher ID: 10.1177_1756286418774254
                DOI: 10.1177/1756286418774254
                PMC ID: 5968660
                SO-VID: b053ba48-3dd1-438c-a65b-85b648c1095f
                Copyright © © The Author(s), 2018
                License:

                This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License ( http://www.creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages ( https://us.sagepub.com/en-us/nam/open-access-at-sage).

                History
                Date received : 23 February 2018
                Date accepted : 10 April 2018
                Funding
                Funded by: Hermann and Lilly Schilling foundation for medical research, ;
                Categories
                Subject: Review
                Custom metadata
                cover-date January-December 2018

                Keywords: damps,stroke,microglia,hmgb1,purines,hsp,peroxiredoxin
                Data availability:
                Keywords: damps, stroke, microglia, hmgb1, purines, hsp, peroxiredoxin

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