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      Neuroinflammation and subarachnoid hemorrhage: a revised look at the literature

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          Abstract

          A key topic for aneurysmal subarachnoid hemorrhage is neuroinflammation. Neuroinflammation can predispose to aneurysm formation and rupture. Neuroinflammation can also result from the blood breakdown products after aneurysm rupture. Recent evidence has shown that perpetual neuroinflammation can contribute to vasospasm and hydrocephalus. Targeting neuroinflammation is a novel mechanism for preventing subsequent neurologic sequalae. In this review, we highlight the pathophysiology of aneurysm formation, the neuroinflammatory surge after rupture including the involved cytokines, and ultimately tie in the contributory clinical relevance. In the last sections, we look at the pre-clinical data and novel avenues for further discovery. This paper will be a useful resource to both the clinician and scientific investigator.

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          Structural and functional features of central nervous system lymphatics

          Antoine Louveau, Igor Smirnov, Timothy Keyes … (2015)
          One of the characteristics of the CNS is the lack of a classical lymphatic drainage system. Although it is now accepted that the CNS undergoes constant immune surveillance that takes place within the meningeal compartment 1–3 , the mechanisms governing the entrance and exit of immune cells from the CNS remain poorly understood 4–6 . In searching for T cell gateways into and out of the meninges, we discovered functional lymphatic vessels lining the dural sinuses. These structures express all of the molecular hallmarks of lymphatic endothelial cells, are able to carry both fluid and immune cells from the CSF, and are connected to the deep cervical lymph nodes. The unique location of these vessels may have impeded their discovery to date, thereby contributing to the long-held concept of the absence of lymphatic vasculature in the CNS. The discovery of the CNS lymphatic system may call for a reassessment of basic assumptions in neuroimmunology and shed new light on the etiology of neuroinflammatory and neurodegenerative diseases associated with immune system dysfunction.
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            Macrophage Polarization: Different Gene Signatures in M1(LPS+) vs. Classically and M2(LPS–) vs. Alternatively Activated Macrophages

            Marco Orecchioni, Yanal Ghosheh, Akula Pramod … (2019)
            Macrophages are found in tissues, body cavities, and mucosal surfaces. Most tissue macrophages are seeded in the early embryo before definitive hematopoiesis is established. Others are derived from blood monocytes. The macrophage lineage diversification and plasticity are key aspects of their functionality. Macrophages can also be generated from monocytes in vitro and undergo classical (LPS+IFN-γ) or alternative (IL-4) activation. In vivo, macrophages with different polarization and different activation markers coexist in tissues. Certain mouse strains preferentially promote T-helper-1 (Th1) responses and others Th2 responses. Their macrophages preferentially induce iNOS or arginase and have been called M1 and M2, respectively. In many publications, M1 and classically activated and M2 and alternatively activated are used interchangeably. We tested whether this is justified by comparing the gene lists positively [M1(=LPS+)] or negatively [M2(=LPS–)] correlated with the ratio of IL-12 and arginase 1 in transcriptomes of LPS-treated peritoneal macrophages with in vitro classically (LPS, IFN-γ) vs. alternatively activated (IL-4) bone marrow derived macrophages, both from published datasets. Although there is some overlap between in vivo M1(=LPS+) and in vitro classically activated (LPS+IFN-γ) and in vivo M2(=LPS–) and in vitro alternatively activated macrophages, many more genes are regulated in opposite or unrelated ways. Thus, M1(=LPS+) macrophages are not equivalent to classically activated, and M2(=LPS–) macrophages are not equivalent to alternatively activated macrophages. This fundamental discrepancy explains why most surface markers identified on in vitro generated macrophages do not translate to the in vivo situation. Valid in vivo M1/M2 surface markers remain to be discovered.
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              Guidelines for the management of aneurysmal subarachnoid hemorrhage: a guideline for healthcare professionals from the American Heart Association/american Stroke Association.

              E Connolly, Alejandro A Rabinstein, J Carhuapoma … (2012)
              The aim of this guideline is to present current and comprehensive recommendations for the diagnosis and treatment of aneurysmal subarachnoid hemorrhage (aSAH). A formal literature search of MEDLINE (November 1, 2006, through May 1, 2010) was performed. Data were synthesized with the use of evidence tables. Writing group members met by teleconference to discuss data-derived recommendations. The American Heart Association Stroke Council's Levels of Evidence grading algorithm was used to grade each recommendation. The guideline draft was reviewed by 7 expert peer reviewers and by the members of the Stroke Council Leadership and Manuscript Oversight Committees. It is intended that this guideline be fully updated every 3 years. Evidence-based guidelines are presented for the care of patients presenting with aSAH. The focus of the guideline was subdivided into incidence, risk factors, prevention, natural history and outcome, diagnosis, prevention of rebleeding, surgical and endovascular repair of ruptured aneurysms, systems of care, anesthetic management during repair, management of vasospasm and delayed cerebral ischemia, management of hydrocephalus, management of seizures, and management of medical complications. aSAH is a serious medical condition in which outcome can be dramatically impacted by early, aggressive, expert care. The guidelines offer a framework for goal-directed treatment of the patient with aSAH.
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                Author and article information

                Journal
                Journal ID (nlm-journal-id): 9918419272606676
                Journal ID (pubmed-jr-id): 51790
                Journal ID (nlm-ta): Clin Res Commun
                Journal ID (iso-abbrev): Clin Res Commun
                Title: Clinical research communications
                ISSN (Electronic): 2815-7176
                Publication date Nihms-submitted: 9 July 2022
                Publication date (Print): 2022
                Publication date (Electronic): 1 July 2022
                Publication date PMC-release: 14 July 2022
                Volume: 5
                Issue: 3
                Electronic Location Identifier: 14
                Affiliations
                [1 ]Department of Neurosurgery, University of Florida, Gainesville, FL, U.S.A.
                [2 ]Rosalind Franklin University of Medicine and Science, Chicago, IL, U.S.A.
                [3 ]Department of Biomolecular Sciences, Boise State University, Boise, ID, U.S.A.
                Author notes
                [* ] Corresponding to: Brandon Lucke-Wold, Department of Neurosurgery, University of Florida, Gainesville, McKnight Brain Institute Room L2-100, 1149 South Newell Drive, Gainesville, Florida 32611, U.S.A. Brandon.Lucke-Wold@ 123456neurosurgery.ufl.edu .
                Article
                Manuscript ID: NIHMS1820385
                DOI: 10.53388/crc20220014
                PMC ID: 9280925
                SO-VID: 7776dd7b-8e64-4961-a1ac-413989b321e5
                License:

                This is an open access article under the CC-BY license. ( http://creativecommons.org/licenses/BY/4.0/)

                History
                Categories
                Subject: Article

                Keywords: neuroinflammation,subarachnoid hemorrhage,treatment approach,aneurysm formation
                Data availability:
                Keywords: neuroinflammation, subarachnoid hemorrhage, treatment approach, aneurysm formation

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