The macrophages are present in various compartments of the central nervous system (CNS) where they play significant roles in homeostasis, response to infection and/or injury, and clearance of cellular debris and aggregated proteins. CNS macrophages (MP) include the microglia and the border-associated macrophages (BAMs); the latter include perivascular, choroid plexus, and leptomeningeal macrophages. The cerebrospinal fluid (CSF) also contains macrophages which may either be floating or attached to various surfaces. These phagocytes are influenced by niche-specific signals and mechanical stimuli instructing their phenotypic identities. With the advent of high-throughput genomic technologies including single cell-transcriptomics and epigenomics, the dichotomization of macrophages into M1 and M2 subtypes no longer holds true and the MP paradigm now consists of specific states depending on context. Studying these MP states on transcriptomic, proteomic, and epigenomic levels in the context of health and neurological disease will allow opportunities for therapeutic modulation. Stroke is a pathology whereby microglia and other MP play a significant role in neuroinflammation as well as repair processes.
The primary aim of this Research Topic will be to collect the most recent scientific advances regarding the role of microglia and other CNS macrophages in all the diverse forms of stroke. Microglia and perivascular macrophages have been shown to perform both pro-inflammatory and anti-inflammatory functions following stroke. Our goal is to highlight innovative findings deciphering CNS macrophage functional states in further depth following stroke and clarifying the pathogenic mechanisms which could be the target of therapeutic modulation of these MP and neuroprotective strategies for stroke.
We welcome the submission of any type of manuscript supported by the journal – including original research, brief research reports, reviews, and mini-reviews – that study the CNS MP paradigm in all the diverse forms of stroke (ischemic stroke, intracerebral hemorrhage, or subarachnoid hemorrhage), during the acute, recurrent, or delayed phase. Specific themes include but are not limited to:
- Innate immune landscape comprising of microglia and BAMs in stroke
- Neuroinflammation-related signaling pathways mediated by CNS MP including inflammasome activation
- Transcriptomic and/or proteomic studies involving the MP following stroke
- Novel immune targets and selective therapeutic modulation of pro-inflammatory microglia
- Drug repurposing for immune modulation in stroke
- Role of MP in linking up with adaptive immunity and promoting vascular leakage following stroke
- Resolution of inflammation and tissue repair as mediated by MP
Keywords:
stroke, macrophages, microglia, neuroinflammation
Important Note:
All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
The macrophages are present in various compartments of the central nervous system (CNS) where they play significant roles in homeostasis, response to infection and/or injury, and clearance of cellular debris and aggregated proteins. CNS macrophages (MP) include the microglia and the border-associated macrophages (BAMs); the latter include perivascular, choroid plexus, and leptomeningeal macrophages. The cerebrospinal fluid (CSF) also contains macrophages which may either be floating or attached to various surfaces. These phagocytes are influenced by niche-specific signals and mechanical stimuli instructing their phenotypic identities. With the advent of high-throughput genomic technologies including single cell-transcriptomics and epigenomics, the dichotomization of macrophages into M1 and M2 subtypes no longer holds true and the MP paradigm now consists of specific states depending on context. Studying these MP states on transcriptomic, proteomic, and epigenomic levels in the context of health and neurological disease will allow opportunities for therapeutic modulation. Stroke is a pathology whereby microglia and other MP play a significant role in neuroinflammation as well as repair processes.
The primary aim of this Research Topic will be to collect the most recent scientific advances regarding the role of microglia and other CNS macrophages in all the diverse forms of stroke. Microglia and perivascular macrophages have been shown to perform both pro-inflammatory and anti-inflammatory functions following stroke. Our goal is to highlight innovative findings deciphering CNS macrophage functional states in further depth following stroke and clarifying the pathogenic mechanisms which could be the target of therapeutic modulation of these MP and neuroprotective strategies for stroke.
We welcome the submission of any type of manuscript supported by the journal – including original research, brief research reports, reviews, and mini-reviews – that study the CNS MP paradigm in all the diverse forms of stroke (ischemic stroke, intracerebral hemorrhage, or subarachnoid hemorrhage), during the acute, recurrent, or delayed phase. Specific themes include but are not limited to:
- Innate immune landscape comprising of microglia and BAMs in stroke
- Neuroinflammation-related signaling pathways mediated by CNS MP including inflammasome activation
- Transcriptomic and/or proteomic studies involving the MP following stroke
- Novel immune targets and selective therapeutic modulation of pro-inflammatory microglia
- Drug repurposing for immune modulation in stroke
- Role of MP in linking up with adaptive immunity and promoting vascular leakage following stroke
- Resolution of inflammation and tissue repair as mediated by MP
Keywords:
stroke, macrophages, microglia, neuroinflammation
Important Note:
All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.