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      The Role of Mast Cells in Stroke

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          Abstract

          Mast cells (MCs) are densely granulated perivascular resident cells of hematopoietic origin. Through the release of preformed mediators stored in their granules and newly synthesized molecules, they are able to initiate, modulate, and prolong the immune response upon activation. Their presence in the central nervous system (CNS) has been documented for more than a century. Over the years, MCs have been associated with various neuroinflammatory conditions of CNS, including stroke. They can exacerbate CNS damage in models of ischemic and hemorrhagic stroke by amplifying the inflammatory responses and promoting brain–blood barrier disruption, brain edema, extravasation, and hemorrhage. Here, we review the role of these peculiar cells in the pathophysiology of stroke, in both immature and adult brain. Further, we discuss the role of MCs as potential targets for the treatment of stroke and the compounds potentially active as MCs modulators.

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          Spontaneous subarachnoid haemorrhage

          Tom A. Schweizer, R. Loch Macdonald (2017)
          Subarachnoid haemorrhage is an uncommon and severe subtype of stroke affecting patients at a mean age of 55 years, leading to loss of many years of productive life. The rupture of an intracranial aneurysm is the underlining cause in 85% of cases. Survival from aneurysmal subarachnoid haemorrhage has increased by 17% in the past few decades, probably because of better diagnosis, early aneurysm repair, prescription of nimodipine, and advanced intensive care support. Nevertheless, survivors commonly have cognitive impairments, which in turn affect patients' daily functionality, working capacity, and quality of life. Additionally, those deficits are frequently accompanied by mood disorders, fatigue, and sleep disturbances. Management requires specialised neurological intensive care units and multidisciplinary clinical expertise, which is better provided in high-volume centres. Many clinical trials have been done, but only two interventions are shown to improve outcome. Challenges that remain relate to prevention of subarachnoid haemorrhage by improved screening and development of lower-risk methods to repair or stabilise aneurysms that have not yet ruptured. Multicentre cooperative efforts might increase the knowledge that can be gained from clinical trials, which is often limited by small studies with differing criteria and endpoints that are done in single centres. Outcome assessments that incorporate finer assessment of neurocognitive function and validated surrogate imaging or biomarkers for outcome could also help to advance the specialty.
          Article 0 comments Cited 394 times – based on 0 reviews     Review now
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            Inflammation in intracerebral hemorrhage: from mechanisms to clinical translation.

            Yu. Zhou, Yanchun Wang, Jian Wang … (2014)
            Intracerebral hemorrhage (ICH) accounts for 10-15% of all strokes and is associated with high mortality and morbidity. Currently, no effective medical treatment is available to improve functional outcomes in patients with ICH. Potential therapies targeting secondary brain injury are arousing a great deal of interest in translational studies. Increasing evidence has shown that inflammation is the key contributor of ICH-induced secondary brain injury. Inflammation progresses in response to various stimuli produced after ICH. Hematoma components initiate inflammatory signaling via activation of microglia, subsequently releasing proinflammatory cytokines and chemokines to attract peripheral inflammatory infiltration. Hemoglobin (Hb), heme, and iron released after red blood cell lysis aggravate ICH-induced inflammatory injury. Danger associated molecular patterns such as high mobility group box 1 protein, released from damaged or dead cells, trigger inflammation in the late stage of ICH. Preclinical studies have identified inflammatory signaling pathways that are involved in microglial activation, leukocyte infiltration, toll-like receptor (TLR) activation, and danger associated molecular pattern regulation in ICH. Recent advances in understanding the pathogenesis of ICH-induced inflammatory injury have facilitated the identification of several novel therapeutic targets for the treatment of ICH. This review summarizes recent progress concerning the mechanisms underlying ICH-induced inflammation. We focus on the inflammatory signaling pathways involved in microglial activation and TLR signaling, and explore potential therapeutic interventions by targeting the removal of hematoma components and inhibition of TLR signaling. Copyright © 2013 Elsevier Ltd. All rights reserved.
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              Mast cells in the development of adaptive immune responses.

              Stephen J. Galli, Susumu Nakae, Mindy Tsai (2005)
              Mast cells are so widely recognized as critical effector cells in allergic disorders and other immunoglobulin E-associated acquired immune responses that it can be difficult to think of them in any other context. However, mast cells also can be important as initiators and effectors of innate immunity. In addition, mast cells that are activated during innate immune responses to pathogens, or in other contexts, can secrete products and have cellular functions with the potential to facilitate the development, amplify the magnitude or regulate the kinetics of adaptive immune responses. Thus, mast cells may influence the development, intensity and duration of adaptive immune responses that contribute to host defense, allergy and autoimmunity, rather than simply functioning as effector cells in these settings.
              Article 0 comments Cited 255 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Cells
                Journal ID (iso-abbrev): Cells
                Journal ID (publisher-id): cells
                Title: Cells
                Publisher: MDPI
                ISSN (Electronic): 2073-4409
                Publication date (Electronic): 10 May 2019
                Publication date Collection: May 2019
                Volume: 8
                Issue: 5
                Electronic Location Identifier: 437
                Affiliations
                Department of Molecular and Translational Medicine, University of Brescia, Viale Europa 11, 25123 Brescia, Italy; v.porrini@ 123456unibs.it (V.P.); marina.benarese@ 123456unibs.it (M.B.); marina.pizzi@ 123456unibs.it (M.P.)
                Author notes
                [* ]Correspondence: edoardo.parrella@ 123456unibs.it ; Tel.: +39-030-3717502
                Author information
                https://orcid.org/0000-0003-0365-5144
                https://orcid.org/0000-0001-8222-155X
                Article
                Publisher ID: cells-08-00437
                DOI: 10.3390/cells8050437
                PMC ID: 6562540
                PubMed ID: 31083342
                SO-VID: ec335691-1526-4fd7-8937-a44ebe6fb845
                Copyright © © 2019 by the authors.
                License:

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 01 April 2019
                Date accepted : 07 May 2019
                Categories
                Subject: Review

                Keywords: mast cells,stroke,neonatal hypoxic-ischemic brain injury,ischemic stroke,brain ischemia,intracerebral hemorrhage,subarachnoid hemorrhage,blood–brain barrier,inflammation
                Data availability:
                Keywords: mast cells, stroke, neonatal hypoxic-ischemic brain injury, ischemic stroke, brain ischemia, intracerebral hemorrhage, subarachnoid hemorrhage, blood–brain barrier, inflammation

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