The Regulation of the CNS Innate Immune Response Is Vital for the Restoration of Tissue Homeostasis (Repair) after Acute Brain Injury: A Brief Review

Griffiths, Mark; Gasque, Philippe; Neal, James

doi:10.4061/2010/151097

Cited by 45 publications

(42 citation statements)

References 190 publications

(341 reference statements)

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“…Previous in silico analyses suggested that inflammatory response markers are able to differentiate patients with SZ or BD (Griffiths et al, 2010;Ricklin et al, 2010). A systematic meta-analysis of 13 studies reviewed evidence of peripheral cytokine alterations in BD and found differences between patients and controls and between phases of disease within patients (Munkholm et al, 2013), suggesting that different symptoms are related to activation of different processes within the cell.…”

Section: Discussionmentioning

confidence: 98%

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Innate immune response is differentially dysregulated between bipolar disease and schizophrenia

Baumont

Maschietto

Lima

et al. 2015

Schizophrenia Research

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Schizophrenia (SZ) and bipolar disorder (BD) are severe psychiatric conditions with a neurodevelopmental component. Genetic findings indicate the existence of an overlap in genetic susceptibility across the disorders. Also, image studies provide evidence for a shared neurobiological basis, contributing to a dimensional diagnostic approach. This study aimed to identify the molecular mechanisms that differentiate SZ and BD patients from health controls but also that distinguish both from health individuals. Comparison of gene expression profiling in post-mortem brains of both disorders and health controls (30 cases), followed by a further comparison between 29 BD and 29 SZ revealed 28 differentially expressed genes. These genes were used in co-expression analysesthat revealed the pairs CCR1/SERPINA1, CCR5/HCST, C1QA/CD68, CCR5/S100A11 and SERPINA1/TLR1 as presenting the most significant difference in co-expression between SZ and BD. Next, a protein-protein interaction (PPI) network using the 28 differentially expressed genes as seeds revealed CASP4, TYROBP, CCR1, SERPINA1, CCR5 and C1QA as having a central role in the diseases manifestation. Both co-expression and network topological analyses pointed to genes related to microglia functions. Based on this data, we suggest that differences between SZ and BP are due to genes involved with response to stimulus, defense response, immune system process and response to stress biological processes, all having a role in the communication of environmental factors to the cells and associated to microglia.

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Section: Discussionmentioning

confidence: 98%

“…Another protein expressed in microglial cells is AIF1, a marker of activated macrophages (Fukui et al, 2012). SERPIN1 has an important role as a self-defense protein that modulates the activation of microglia (Griffiths et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

Innate immune response is differentially dysregulated between bipolar disease and schizophrenia

Baumont

Maschietto

Lima

et al. 2015

Schizophrenia Research

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“…Reactive astrocytes are also capable of inducing T-cell apoptosis and may thereby control the spread of peripheral lymphocyte-mediated inflammation following severe TBI. For example, following TBI, reactive astrocytes upregulate CD95 and CD95R to induce lymphocyte apoptosis through a CD95/CD95R-dependent mechanism, though astrocytes themselves remain protected (Bechmann et al, 2000; Bechmann et al, 2002; Griffiths et al, 2010). …”

Section: Scar-forming Reactive Astrocytes Form Functional Barriers Armentioning

confidence: 99%

Astrocyte roles in traumatic brain injury

Burda

Bernstein

Sofroniew

2016

Experimental Neurology

606

479

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Astrocytes sense changes in neural activity and extracellular space composition. In response, they exert homeostatic mechanisms critical for maintaining neural circuit function, such as buffering neurotransmitters, modulating extracellular osmolarity and calibrating neurovascular coupling. In addition to upholding normal brain activities, astrocytes respond to diverse forms of brain injury with heterogeneous and progressive changes of gene expression, morphology, proliferative capacity and function that are collectively referred to as reactive astrogliosis. Traumatic brain injury (TBI) sets in motion complex events in which noxious mechanical forces cause tissue damage and disrupt central nervous system (CNS) homeostasis, which in turn trigger diverse multi-cellular responses that evolve over time and can lead either to neural repair or secondary cellular injury. In response to TBI, astrocytes in different cellular microenvironments tune their reactivity to varying degrees of axonal injury, vascular disruption, ischemia and inflammation. Here we review different forms of TBI-induced astrocyte reactivity and the functional consequences of these responses for TBI pathobiology. Evidence regarding astrocyte contribution to post-traumatic tissue repair and synaptic remodeling is examined, and the potential for targeting specific aspects of astrogliosis to ameliorate TBI sequelae is considered.

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“…The Wld s mouse, which displays a delayed Wallerian degeneration phenotype similar to SARM −/− mice, is also deficient in cytokine production suggesting that the processes are intricately linked (12). In addition to promoting repair of damaged brain tissue, glial activation and cytokine production in the CNS may injure bystander cells (13, 14). In other organs, this collateral damage is typically reversible, owing to the regenerative capacity of the tissue, but repopulation of cells is limited in the CNS (15).…”

Section: Introductionmentioning

confidence: 99%

SARM Is Required for Neuronal Injury and Cytokine Production in Response to Central Nervous System Viral Infection

Hou

Banerjee

Thomas³

et al. 2013

The Journal of Immunology

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Four of the five members of the Toll-interleukin-1 receptor (TIR) domain-containing adaptor family are required for signaling downstream of Toll-like receptors, promoting innate immune responses against different pathogens. However, the role of the fifth member of this family, sterile alpha and TIR-domain containing 1 (SARM), is unclear. SARM is expressed primarily in the central nervous system where it is required for axonal death. Studies in C.elegans have also shown a role for SARM in innate immunity. To clarify the role of mammalian SARM in innate immunity, we infected SARM−/− mice with a number of bacterial and viral pathogens. SARM−/− mice show normal responses to Listeria monocytogenes, Mycobacterium tuberculosis (Mtb), and influenza virus, but show dramatic protection from death after CNS infection with vesicular stomatitis virus (VSV). Protection correlates with reduced CNS injury and cytokine production by non-hematopoietic cells, suggesting that SARM is a positive regulator of cytokine production. Neurons and microglia are the predominant source of cytokines in vivo, supporting a role for SARM as a link between neuronal injury and innate immunity.

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The Regulation of the CNS Innate Immune Response Is Vital for the Restoration of Tissue Homeostasis (Repair) after Acute Brain Injury: A Brief Review

Cited by 45 publications

References 190 publications

Innate immune response is differentially dysregulated between bipolar disease and schizophrenia

Innate immune response is differentially dysregulated between bipolar disease and schizophrenia

Astrocyte roles in traumatic brain injury

SARM Is Required for Neuronal Injury and Cytokine Production in Response to Central Nervous System Viral Infection

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