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      The gut microbiome primes a cerebroprotective immune response after stroke

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          Abstract

          Microbiome alterations have been shown to affect stroke outcome. However, to what extent the presence of a gut microbiome per se is affecting post-stroke neuroinflammation has not been tested. By comparing germfree mice with recolonized (Ex-GF) and conventional SPF mice, we were able to demonstrate that bacterial colonization reduces stroke volumes. Bacterial colonization increased cerebral expression of cytokines as well as microglia/macrophage cell counts in contrast to improved stroke outcome. Interestingly, the microbiome-mediated brain protection was absent in lymphocyte-deficient mice. These findings support the concept of lymphocyte-driven protective neuroinflammation after stroke under control of the microbiome.

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          Thromboinflammation in Stroke Brain Damage.

          Simon F. De Meyer, Frederik Denorme, Friederike Langhauser … (2016)
          Article 0 comments Cited 129 times – based on 0 reviews     Review now
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            Microbiota differences between commercial breeders impacts the post-stroke immune response.

            Arthur Liesz, Vikramjeet Singh, Corinne Benakis … (2017)
            Experimental reproducibility between laboratories is a major translational obstacle worldwide, particularly in studies investigating immunomodulatory therapies in relation to brain disease. In recent years increasing attention has been drawn towards the gut microbiota as a key factor in immune cell polarization. Moreover, manipulation of the gut microbiota has been found effective in a diverse range of brain disorders. Within this study we aimed to test the impact of microbiota differences between mice from different sources on the post-stroke neuroinflammatory response. With this rationale, we have investigated the correlation between microbiota differences and the immune response in mice from three commercial breeders with the same genetic background (C57BL/6). While overall bacterial load was comparable, we detected substantial differences in species diversity and microbiota composition on lower taxonomic levels. Specifically, we investigated segmented filamentous bacteria (SFB)-which have been shown to promote T cell polarization-and found that they were absent in mice from one breeder but abundant in others. Our experiments revealed a breeder specific correlation between SFB presence and the ratio of Treg to Th17 cells. Moreover, recolonization of SFB-negative mice with SFB resulted in a T cell shift which mimicked the ratios found in SFB-positive mice. We then investigated the response to a known experimental immunotherapeutic approach, CD28 superagonist (CD28SA), which has been previously shown to expand the Treg population. CD28SA treatment had differing effects between mice from different breeders and was found to be ineffective at inducing Treg expansion in SFB-free mice. These changes directly corresponded to stroke outcome as mice lacking SFB had significantly larger brain infarcts. This study demonstrates the major impact of microbiota differences on T cell polarization in mice during ischemic stroke conditions, and following immunomodulatory therapies.
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              Protective autoimmunity and neuroprotection in inflammatory and noninflammatory neurodegenerative diseases.

              Jonathan Kipnis, Michal Schwartz (2005)
              Autoimmune diseases are traditionally viewed as an outcome of a malfunctioning of the immune system, in which an individual's immune system reacts against the body's own proteins. In multiple sclerosis (MS), a disease of the white matter of the central nervous system (CNS), the attack is directed against myelin proteins. In this article we summarize a paradigm shift proposed by us in the perception of autoimmune disease. Observations by our group indicating that an autoimmune response is the body's mechanism for coping with CNS damage led us to suggest that all individuals are apparently endowed with a purposeful autoimmune response to CNS injuries, but have only limited inherent ability to control this response so that its effect will be beneficial. In animals susceptible to autoimmune diseases, the same autoimmune T cells are responsible both for neuroprotection and for disease development; the timing and strength of their activity will determine which of these effects is expressed. Individuals with non-inflammatory neurodegenerative diseases need a heightened autoimmunity. We discovered that autoimmunity could be boosted without risk of disease induction, even in susceptible strains, by the use of Copolymer-1 (Copaxone(R)), a weak agonist of a wide range of self-reactive T cells. Here we summarize the basic findings that led us to formulate the concept of protective autoimmunity, the mechanisms underlying its constitutive presence and its on/off regulation, and its therapeutic implications. We also offer an explanation for the commonly observed presence of cells and antibodies directed against self-components in healthy individuals.
              Article 0 comments Cited 14 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Title: Journal of Cerebral Blood Flow & Metabolism
                Abbreviated Title: J Cereb Blood Flow Metab
                Publisher: SAGE Publications
                ISSN (Print): 0271-678X
                ISSN (Electronic): 1559-7016
                Publication date Created: July 07 2017
                Publication date Created: August 2018
                Publication date (Electronic): May 30 2018
                Publication date (Print): August 2018
                Volume: 38
                Issue: 8
                Pages: 1293-1298
                Affiliations
                [1 ]Institute for Stroke and Dementia Research, Klinikum der Universität München, Munich, Germany
                [2 ]Munich Cluster for Systems Neurology (SyNergy), Munich, Germany
                Article
                DOI: 10.1177/0271678X18780130
                PMC ID: 6092773
                PubMed ID: 29846130
                SO-VID: 7c0456de-5e06-4653-91c1-d3697b994397
                Copyright © © 2018
                License:

                http://journals.sagepub.com/page/policies/text-and-data-mining-license

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