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Topic: The Immune System and Inflammation in Stroke

A special issue of Neuroimmunology and Neuroinflammation

ISSN 2349-6142 (Online), ISSN 2347-8659 (Print)

Submission deadline: 30 Apr 2020

Guest Editor(s)

  • Dr. Christiane Charriaut-Marlangue
    NeuroDiderot - INSERM U1141. Université Paris Diderot, Sorbonne Paris Cité, Hôpital Robert Debré, 48 boulevard Sérurier, Paris, France.


Special Issue Introduction

Stroke is a disorder affecting all age groups, particularly those at opposite ends of the age spectrum, with an incidence of 1/2800 to 1/5000 life infant births, and more than 6 million cases every year in adult stroke, respectively. To date, there is still no effective treatment that increases the survival rate or improves the quality of life both during the neonatal period (the first 28 days of life) and/or in adulthood. During the last decade, the male sex appeared to be a determinant factor, not only in the worse outcome (during the first 40-50 years of life) but also in response to cellular and molecular pathways activated in different cerebral area involved in behavioral functions.
Stroke triggers dysfunction in several pathways, with multiple final outcomes which include multiple paths to death or to recovery. The activation of resident microglial cells, alongside the infiltration of peripheral macrophages, represents a central inflammatory response to ischemic stroke leading to secondary injury cascade associated with neuronal death. Microglia/macrophages are the main players in propagating inflammation to tissues neighboring the core site of injury. They perform this task through the production of inflammatory mediators including cytokines and chemokines.
For this special issue of the journal, we request submission of manuscripts concerning the molecular pathways in microglia/macrophage and immune (infiltration of peripheral myeloid cells including polymorphonuclear, lymphocytes and monocytes) responses after stroke in pre-clinical studies.
Submissions especially (but not exclusively) on the following topics are welcomed: 
- specific microglial gene and region differences between male and female brains;
- specific microglial responses according to the developmental stage of ischemic animals;
- specific microglial responses according to rodent species used in the stroke models.
These data may highlight the development of add-on sex-specific therapeutically strategies in stroke units.


Lesion, ischemic core, ischemic peri-infarct, macrophage, microglia, neuroinflammation, sex-differences, polymorphonuclear, lymphocytes, monocytes

Submission Deadline

30 Apr 2020

Submission Information

For Author Instructions, please refer to http://nnjournal.net/pages/view/author_instructions
For Online Submission, please login at https://oaemesas.com/login?JournalId=nn&SpecialIssueId=318
Submission Deadline: 30 Apr 2020
Contacts: Orla Meng, Managing Editor, editor002@nnjournal.net


Planned Papers

Type: Original Article

Title: A study on Mer- tyrosine kinase (MerTK)

Authors: Ertugrul Kilic

Affiliations: Department of Physiology, Faculty of Medicine, Istanbul Medipol University, Istanbul 34810, Turkey.

Abstract: MerTK three receptor kinase, Tyro3, Axl and Mer (TAM) and their ligands Gas6 and Protein S, are robust negative regulators of innate immune response. In a series of studies in which TAM locus is genetically removed from mice, functional mechanisms of TAM receptors in the development of immune response and phagocytosis of apoptotic cells were investigated. After the phagocytosis of apoptotic cells and induction of T cell-dependent adaptive immune response, ligand-dependent TAM signals inhibit long-term inflammation by reducing the proinflammatory cytokine production. MerTK has the highest affinity in phagocytotic processes among the TAM family. Even though it is well-known that MerTK plays a role in phagocytosis of apoptotic cells in the brain and other tissues, the knowledge regarding the pathophysiological processes following brain injury is limited and there is a huge demand in the literature about this issue. To this end, we are planning to investigate the role of MerTK in the reorganization of the brain following brain injury.

Type: Review

Title: Resolution of inflammation and repair after ischemic brain injury

Authors: Akihiko Yoshimura1, Minako Ito1,2

Affiliations: 1Department of Microbiology and Immunology, Keio University School of Medicine, Tokyo 160-8582, Japan.
2Division of Allergy and Immunology, Medical Institute of Bioregulation, Kyushu University, Fukuoka 812-8582, Japan.

Abstract: After ischemic stroke, the proinflammatory molecules known as DAMPs (danger-associated molecular patterns), secreted by damaged brain cells, recruit and activate immune cells (neutrophils, macrophages, and lymphocytes) and elicit innate and adaptive immunity. During the acute phase, from Day 1 to Day 3 after stroke onset, macrophages play major roles in the progression of inflammation, which promotes the destruction of brain tissue. During the recovery phase, from Days 3-4 to Day 7 after stroke onset, the infiltrating macrophages switch to repairing macrophages, which clear the DAMPs and promote tissue repair by producing neurotrophic factors. Adaptive immunity during the late or chronic phase (> Day 7) of stroke has not been well investigated. However, recent studies have indicated that antigen-specific T cells, especially regulatory T cells (Tregs), play major roles in neural repair. This review mostly focuses on the resolution of inflammation and tissue repair by macrophages and Tregs.

Type: Review

Title: Microglial response after brain stroke

Authors: Olivier Wurtz

Affiliations: Institut de Recherche et d'Innovation Biomédicale (IRIB), Université de Rouen, Rouen 76821, France.

Abstract: Despite years of intense research, brain stroke remains a leading cause of death and long-term disabilities worldwide. Acute ischemic stroke, the most prevalent stroke subtype, results from a thrombus responsible for the sudden blockage of blood flow in a given cerebral territory. The breakdown of oxygen and nutrients supply initiates a cascade of pathophysiological events evolving in time and space, leading to a massive neuronal cell death and consecutive neurological deficits. Among the post-ischemic mechanisms, inflammation is a complex process initiated early after stroke onset and sustained over weeks, exerting both detrimental and beneficial effects. Microglial cell population, a unique immunocompetent compartment in the brain parenchyma, tightly controls the neuroinflammatory response and becomes an interesting therapeutical target. Initially thought to increase neuronal cell death through proinflammatory mediator secretion and reactive species production, numerous studies also report the neuroprotective role of microglia promoting neuronal trophic support and tissue repair. Hence, the phenotype of the microglial response can evolve according to environmental cues and timing after brain injury. Here, we focus on the duality of this microglial response, its versatility and dynamic in relation with the evolution of signals available during the different phases of the disease. We discuss the relationships between the phenotype of the microglial response and the cellular processes, which can support detrimental and beneficial consequences. Understanding the signals that drive microglial cell polarization will allow the development of therapeutical strategies designed to skew, rather than simply inhibiting, the post-ischemic microglial response toward its neuroprotective phenotype. Definitely, such immunomodulatory strategies targeting microglial responses in the early phase as well as in the late phase of stroke could contribute to improving functional recovery in stroke victims.

Published Articles

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