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Article ; Online: Microglia shield the murine brain from damage mediated by the cytokines IL-6 and IFN-α.

West, Phillip K / Viengkhou, Barney / Campbell, Iain L / Hofer, Markus J

2022 Volume 13, Page(s) 1036799

Abstract: Sustained production of elevated levels of the cytokines interleukin (IL)-6 or interferon (IFN)-α in the central nervous system (CNS) is detrimental and directly contributes to the pathogenesis of neurological diseases such as neuromyelitis optica ... ...

Abstract	Sustained production of elevated levels of the cytokines interleukin (IL)-6 or interferon (IFN)-α in the central nervous system (CNS) is detrimental and directly contributes to the pathogenesis of neurological diseases such as neuromyelitis optica spectrum disorders or cerebral interferonopathies, respectively. Using transgenic mice with CNS-targeted production of IL-6 (GFAP-IL6) or IFN-α (GFAP-IFN), we have recently demonstrated that microglia are prominent target and effector cells and mount stimulus-specific responses to these cytokines. In order to further clarify the phenotype and function of these cells, we treated GFAP-IL6 and GFAP-IFN mice with the CSF1R inhibitor PLX5622 to deplete microglia. We examined their ability to recover from acute microglia depletion, as well as the impact of chronic microglia depletion on the progression of disease. Following acute depletion in the brains of GFAP-IL6 mice, microglia repopulation was enhanced, while in GFAP-IFN mice, microglia did not repopulate the brain. Furthermore, chronic CSF1R inhibition was detrimental to the brain of GFAP-IL6 and GFAP-IFN mice and gave rise to severe CNS calcification which strongly correlated with the absence of microglia. In addition, PLX5622-treated GFAP-IFN mice had markedly reduced survival. Our findings provide evidence for novel microglia functions to protect against IFN-α-mediated neurotoxicity and neuronal dysregulation, as well as restrain calcification as a result of both IL-6- and IFN-α-induced neuroinflammation. Taken together, we demonstrate that CSF1R inhibition may be an undesirable target for therapeutic treatment of neuroinflammatory diseases that are driven by elevated IL-6 and IFN-α production.
MeSH term(s)	Animals ; Mice ; Interleukin-6/metabolism ; Microglia/metabolism ; Cytokines ; Brain/metabolism ; Interferon-alpha ; Mice, Transgenic
Chemical Substances	Interleukin-6 ; Cytokines ; PLX5622 ; Interferon-alpha
Language	English
Publishing date	2022-10-28
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2022.1036799
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Article ; Online: Strawberry notch homolog 2 regulates the response to interleukin-6 in the central nervous system.

Syme, Taylor E / Grill, Magdalena / Hayashida, Emina / Viengkhou, Barney / Campbell, Iain L / Hofer, Markus J

Journal of neuroinflammation

2022 Volume 19, Issue 1, Page(s) 126

Abstract: Background: The cytokine interleukin-6 (IL-6) modulates a variety of inflammatory processes and, context depending, can mediate either pro- or anti-inflammatory effects. Excessive IL-6 signalling in the brain is associated with chronic inflammation ... ...

Abstract	Background: The cytokine interleukin-6 (IL-6) modulates a variety of inflammatory processes and, context depending, can mediate either pro- or anti-inflammatory effects. Excessive IL-6 signalling in the brain is associated with chronic inflammation resulting in neurodegeneration. Strawberry notch homolog 2 (Sbno2) is an IL-6-regulated gene whose function is largely unknown. Here we aimed to address this issue by investigating the impact of Sbno2 disruption in mice with IL-6-mediated neuroinflammation. Methods: Mice with germline disruption of Sbno2 (Sbno2 Results: We found Sbno2 Conclusion: Based on these results, we propose a role for SBNO2 as a novel negative feedback regulator of IL-6 that restrains the excessive inflammatory actions of this cytokine in the brain.
MeSH term(s)	Animals ; Astrocytes/metabolism ; Brain/metabolism ; Cytokines/metabolism ; Interleukin-6/metabolism ; Mice
Chemical Substances	Cytokines ; Interleukin-6
Language	English
Publishing date	2022-05-27
Publishing country	England
Document type	Journal Article
ZDB-ID	2156455-3
ISSN	1742-2094 ; 1742-2094
ISSN (online)	1742-2094
ISSN	1742-2094
DOI	10.1186/s12974-022-02475-1
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Article ; Online: Interferon-α receptor antisense oligonucleotides reduce neuroinflammation and neuropathology in a mouse model of cerebral interferonopathy.

Viengkhou, Barney / Hong, Christine / Mazur, Curt / Damle, Sagar / Gallo, Nicholas B / Fang, Terry C / Henry, Kate / Campbell, Iain L / Kamme, Fredrik / Hofer, Markus J

The Journal of clinical investigation

2024 Volume 134, Issue 4

Abstract: Chronic and elevated levels of the antiviral cytokine IFN-α in the brain are neurotoxic. This is best observed in patients with genetic cerebral interferonopathies such as Aicardi-Goutières syndrome. Cerebral interferonopathies typically manifest in ... ...

Abstract	Chronic and elevated levels of the antiviral cytokine IFN-α in the brain are neurotoxic. This is best observed in patients with genetic cerebral interferonopathies such as Aicardi-Goutières syndrome. Cerebral interferonopathies typically manifest in early childhood and lead to debilitating disease and premature death. There is no cure for these diseases with existing treatments largely aimed at managing symptoms. Thus, an effective therapeutic strategy is urgently needed. Here, we investigated the effect of antisense oligonucleotides targeting the murine IFN-α receptor (Ifnar1 ASOs) in a transgenic mouse model of cerebral interferonopathy. Intracerebroventricular injection of Ifnar1 ASOs into transgenic mice with brain-targeted chronic IFN-α production resulted in a blunted cerebral interferon signature, reduced neuroinflammation, restoration of blood-brain barrier integrity, absence of tissue destruction, and lessened neuronal damage. Remarkably, Ifnar1 ASO treatment was also effective when given after the onset of neuropathological changes, as it reversed such disease-related features. We conclude that ASOs targeting the IFN-α receptor halt and reverse progression of IFN-α-mediated neuroinflammation and neurotoxicity, opening what we believe to be a new and promising approach for the treatment of patients with cerebral interferonopathies.
MeSH term(s)	Child, Preschool ; Humans ; Mice ; Animals ; Neuroinflammatory Diseases ; Oligonucleotides, Antisense/genetics ; Oligonucleotides, Antisense/pharmacology ; Nervous System Diseases ; Interferon-alpha/genetics ; Mice, Transgenic ; Interferon Type I
Chemical Substances	Oligonucleotides, Antisense ; Interferon-alpha ; Interferon Type I
Language	English
Publishing date	2024-01-09
Publishing country	United States
Document type	Journal Article
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI169562
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Article ; Online: PLX5622 Reduces Disease Severity in Lethal CNS Infection by Off-Target Inhibition of Peripheral Inflammatory Monocyte Production.

Spiteri, Alanna G / Ni, Duan / Ling, Zheng Lung / Macia, Laurence / Campbell, Iain L / Hofer, Markus J / King, Nicholas J C

Frontiers in immunology

2022 Volume 13, Page(s) 851556

Abstract: PLX5622 is a CSF-1R inhibitor and microglia-depleting reagent, widely used to investigate the biology of this central nervous system (CNS)-resident myeloid population, but the indirect or off-target effects of this agent remain largely unexplored. In a ... ...

Abstract	PLX5622 is a CSF-1R inhibitor and microglia-depleting reagent, widely used to investigate the biology of this central nervous system (CNS)-resident myeloid population, but the indirect or off-target effects of this agent remain largely unexplored. In a murine model of severe neuroinflammation induced by West Nile virus encephalitis (WNE), we showed PLX5622 efficiently depleted both microglia and a sub-population of border-associated macrophages in the CNS. However, PLX5622 also significantly depleted mature Ly6C
MeSH term(s)	Animals ; Mice ; Microglia ; Monocytes ; Organic Chemicals ; Receptors, Colony-Stimulating Factor/metabolism ; Severity of Illness Index ; West Nile Fever
Chemical Substances	Organic Chemicals ; PLX5622 ; Receptors, Colony-Stimulating Factor
Language	English
Publishing date	2022-03-25
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2022.851556
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Article ; Online: Mobilisation of deep crustal sulfide melts as a first order control on upper lithospheric metallogeny.

Holwell, David A / Fiorentini, Marco L / Knott, Thomas R / McDonald, Iain / Blanks, Daryl E / Campbell McCuaig, T / Gorczyk, Weronika

Nature communications

2022 Volume 13, Issue 1, Page(s) 573

Abstract: Magmatic arcs are terrestrial environments where lithospheric cycling and recycling of metals and volatiles is enhanced. However, the first-order mechanism permitting the episodic fluxing of these elements from the mantle through to the outer Earth's ... ...

Abstract	Magmatic arcs are terrestrial environments where lithospheric cycling and recycling of metals and volatiles is enhanced. However, the first-order mechanism permitting the episodic fluxing of these elements from the mantle through to the outer Earth's spheres has been elusive. To address this knowledge gap, we focus on the textural and minero-chemical characteristics of metal-rich magmatic sulfides hosted in amphibole-olivine-pyroxene cumulates in the lowermost crust. We show that in cumulates that were subject to increasing temperature due to prolonged mafic magmatism, which only occurs episodically during the complex evolution of any magmatic arc, Cu-Au-rich sulfide can exist as liquid while Ni-Fe rich sulfide occurs as a solid phase. This scenario occurs within a 'Goldilocks' temperature zone at ~1100-1200 °C, typical of the base of the crust in arcs, which permits episodic fractionation and mobilisation of Cu-Au-rich sulfide liquid into permeable melt networks that may ascend through the lithosphere providing metals for porphyry and epithermal ore deposits.
Language	English
Publishing date	2022-01-31
Publishing country	England
Document type	Journal Article
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-022-28275-y
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Article ; Online: Chronic exposure to IL-6 induces a desensitized phenotype of the microglia.

Recasens, Mireia / Almolda, Beatriz / Pérez-Clausell, Jeús / Campbell, Iain L / González, Berta / Castellano, Bernardo

Journal of neuroinflammation

2021 Volume 18, Issue 1, Page(s) 31

Abstract: Background: When the homeostasis of the central nervous system (CNS) is altered, microglial cells become activated displaying a wide range of phenotypes that depend on the specific site, the nature of the activator, and particularly the microenvironment ...

Abstract	Background: When the homeostasis of the central nervous system (CNS) is altered, microglial cells become activated displaying a wide range of phenotypes that depend on the specific site, the nature of the activator, and particularly the microenvironment generated by the lesion. Cytokines are important signals involved in the modulation of the molecular microenvironment and hence play a pivotal role in orchestrating microglial activation. Among them, interleukin-6 (IL-6) is a pleiotropic cytokine described in a wide range of pathological conditions as a potent inducer and modulator of microglial activation, but with contradictory results regarding its detrimental or beneficial functions. The objective of the present study was to evaluate the effects of chronic IL-6 production on the immune response associated with CNS-axonal anterograde degeneration. Methods: The perforant pathway transection (PPT) paradigm was used in transgenic mice with astrocyte-targeted IL6-production (GFAP-IL6Tg). At 2, 3, 7, 14, and 21 days post-lesion, the hippocampal areas were processed for immunohistochemistry, flow cytometry, and protein microarray. Results: An increase in the microglia/macrophage density was observed in GFAP-IL6Tg animals in non-lesion conditions and at later time-points after PPT, associated with higher microglial proliferation and a major monocyte/macrophage cell infiltration. Besides, in homeostasis, GFAP-IL6Tg showed an environment usually linked with an innate immune response, with more perivascular CD11b Conclusions: Chronic exposure to IL-6 induces a desensitized phenotype of the microglia.
MeSH term(s)	Animals ; Female ; Interleukin-6/metabolism ; Male ; Mice ; Mice, Transgenic ; Microglia ; Nerve Degeneration/metabolism ; Nerve Degeneration/physiopathology ; Perforant Pathway/injuries ; Phenotype
Chemical Substances	Interleukin-6
Language	English
Publishing date	2021-01-22
Publishing country	England
Document type	Journal Article
ISSN	1742-2094
ISSN (online)	1742-2094
DOI	10.1186/s12974-020-02063-1
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Article ; Online: A novel phosphoproteomic landscape evoked in response to type I interferon in the brain and in glial cells.

Viengkhou, Barney / White, Melanie Y / Cordwell, Stuart J / Campbell, Iain L / Hofer, Markus J

Journal of neuroinflammation

2021 Volume 18, Issue 1, Page(s) 237

Abstract: Background: Type I interferons (IFN-I) are key responders to central nervous system infection and injury and are also increased in common neurodegenerative diseases. Their effects are primarily mediated via transcriptional regulation of several hundred ... ...

Abstract	Background: Type I interferons (IFN-I) are key responders to central nervous system infection and injury and are also increased in common neurodegenerative diseases. Their effects are primarily mediated via transcriptional regulation of several hundred interferon-regulated genes. In addition, IFN-I activate several kinases including members of the MAPK and PI3K families. Yet, how changes to the global protein phosphoproteome contribute to the cellular response to IFN-I is unknown. Methods: The cerebral phosphoproteome of mice with brain-targeted chronic production of the IFN-I, IFN-α, was obtained. Changes in phosphorylation were analyzed by ontology and pathway analysis and kinase enrichment predictions. These were verified by phenotypic analysis, immunohistochemistry and immunoblots. In addition, primary murine microglia and astrocytes, the brain's primary IFN-I-responding cells, were acutely treated with IFN-α and the global phosphoproteome was similarly analyzed. Results: We identified widespread protein phosphorylation as a novel mechanism by which IFN-I mediate their effects. In our mouse model for IFN-I-induced neurodegeneration, protein phosphorylation, rather than the proteome, aligned with the clinical hallmarks and pathological outcome, including impaired development, motor dysfunction and seizures. In vitro experiments revealed extensive and rapid IFN-I-induced protein phosphorylation in microglia and astrocytes. Response to acute IFN-I stimulation was independent of gene expression and mediated by a small number of kinase families. The changes in the phosphoproteome affected a diverse range of cellular processes and functional analysis suggested that this response induced an immediate reactive state and prepared cells for subsequent transcriptional responses. Conclusions: Our studies reveal a hitherto unappreciated role for changes in the protein phosphorylation landscape in cellular responses to IFN-I and thus provide insights for novel diagnostic and therapeutic strategies for neurological diseases caused by IFN-I.
MeSH term(s)	Animals ; Brain/drug effects ; Brain/metabolism ; Cells, Cultured ; Female ; Interferon Type I/pharmacology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Microglia/drug effects ; Microglia/metabolism ; Phosphopeptides/genetics ; Phosphopeptides/metabolism ; Phosphorylation/drug effects ; Phosphorylation/physiology ; Proteomics/methods
Chemical Substances	Interferon Type I ; Phosphopeptides
Language	English
Publishing date	2021-10-16
Publishing country	England
Document type	Journal Article
ZDB-ID	2156455-3
ISSN	1742-2094 ; 1742-2094
ISSN (online)	1742-2094
ISSN	1742-2094
DOI	10.1186/s12974-021-02277-x
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Article ; Online: Microglia responses to interleukin-6 and type I interferons in neuroinflammatory disease.

West, Phillip K / Viengkhou, Barney / Campbell, Iain L / Hofer, Markus J

Glia

2019 Volume 67, Issue 10, Page(s) 1821–1841

Abstract: Microglia are the resident macrophages of the central nervous system (CNS). They are a heterogenous, exquisitely responsive, and highly plastic cell population, which enables them to perform diverse roles. They sense and respond to the local production ... ...

Abstract	Microglia are the resident macrophages of the central nervous system (CNS). They are a heterogenous, exquisitely responsive, and highly plastic cell population, which enables them to perform diverse roles. They sense and respond to the local production of many different signals, including an assorted range of cytokines. Microglia respond strongly to interleukin-6 (IL-6) and members of the type I interferon (IFN-I) family, IFN-alpha (IFN-α), and IFN-beta (IFN-β). Although these cytokines are essential in maintaining homeostasis and for activating and regulating immune responses, their chronic production has been linked to the development of distinct human neurological diseases, termed "cerebral cytokinopathies." IL-6 and IFN-α have been identified as key mediators in the pathogenesis of neuroinflammatory disorders including neuromyelitis optica and Aicardi-Goutières syndrome, respectively, whereas IFN-β has an emerging role as a causal factor in age-associated cognitive decline. One of the key features that unites these diseases is the presence of highly reactive microglia. The current understanding is that microglia contribute to the development of cerebral cytokinopathies and represent an important therapeutic target. However, it remains to be resolved whether microglia have beneficial or detrimental effects. Here we review and discuss what is currently known about the microglial response to IL-6 and IFN-I, based on both animal models and clinical studies. Foundational knowledge regarding the microglial response to IL-6 and IFN-I is now being used to devise therapeutic strategies to ameliorate neuroinflammation and promote repair: either through targeting microglia, or by targeting the reduction of CNS levels or downstream biological pathways of IL-6 or IFN-I.
MeSH term(s)	Animals ; Central Nervous System/metabolism ; Central Nervous System Diseases/metabolism ; Central Nervous System Diseases/therapy ; Humans ; Inflammation/metabolism ; Inflammation/therapy ; Interferon Type I/metabolism ; Interleukin-6/metabolism ; Microglia/metabolism
Chemical Substances	Interferon Type I ; Interleukin-6
Language	English
Publishing date	2019-04-29
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	639414-0
ISSN	1098-1136 ; 0894-1491
ISSN (online)	1098-1136
ISSN	0894-1491
DOI	10.1002/glia.23634
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Article ; Online: Mobilisation of deep crustal sulfide melts as a first order control on upper lithospheric metallogeny

David A. Holwell / Marco L. Fiorentini / Thomas R. Knott / Iain McDonald / Daryl E. Blanks / T. Campbell McCuaig / Weronika Gorczyk

Nature Communications, Vol 13, Iss 1, Pp 1-

2022 Volume 12

Abstract: The presence and mobility of metal-rich sulfides in lower crustal magma chambers can act as a gateway for metals to be trapped, or released into ascending magmas that are then able to form upper crustal porphyry copper and gold deposits. ...

Abstract	The presence and mobility of metal-rich sulfides in lower crustal magma chambers can act as a gateway for metals to be trapped, or released into ascending magmas that are then able to form upper crustal porphyry copper and gold deposits.
Keywords	Science ; Q
Language	English
Publishing date	2022-01-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: High-parameter cytometry unmasks microglial cell spatio-temporal response kinetics in severe neuroinflammatory disease.

Spiteri, Alanna G / Terry, Rachel L / Wishart, Claire L / Ashhurst, Thomas M / Campbell, Iain L / Hofer, Markus J / King, Nicholas J C

Journal of neuroinflammation

2021 Volume 18, Issue 1, Page(s) 166

Abstract: Background: Differentiating infiltrating myeloid cells from resident microglia in neuroinflammatory disease is challenging, because bone marrow-derived inflammatory monocytes infiltrating the inflamed brain adopt a 'microglia-like' phenotype. This ... ...

Abstract	Background: Differentiating infiltrating myeloid cells from resident microglia in neuroinflammatory disease is challenging, because bone marrow-derived inflammatory monocytes infiltrating the inflamed brain adopt a 'microglia-like' phenotype. This precludes the accurate identification of either cell type without genetic manipulation, which is important to understand their temporal contribution to disease and inform effective intervention in its pathogenesis. During West Nile virus (WNV) encephalitis, widespread neuronal infection drives substantial CNS infiltration of inflammatory monocytes, causing severe immunopathology and/or death, but the role of microglia in this remains unclear. Methods: Using high-parameter cytometry and dimensionality-reduction, we devised a simple, novel gating strategy to identify microglia and infiltrating myeloid cells during WNV-infection. Validating our strategy, we (1) blocked the entry of infiltrating myeloid populations from peripheral blood using monoclonal blocking antibodies, (2) adoptively transferred BM-derived monocytes and tracked their phenotypic changes after infiltration and (3) labelled peripheral leukocytes that infiltrate into the brain with an intravenous dye. We demonstrated that myeloid immigrants populated only the identified macrophage gates, while PLX5622 depletion reduced all 4 subsets defined by the microglial gates. Results: Using this gating approach, we identified four consistent microglia subsets in the homeostatic and WNV-infected brain. These were P2RY12 Conclusions: Our approach enables detailed kinetic analysis of resident vs infiltrating myeloid cells in a wide range of neuroinflammatory models without non-physiological manipulation. This will more clearly inform potential therapeutic approaches that specifically modulate these cells.
MeSH term(s)	Adoptive Transfer/methods ; Animals ; Antibodies, Monoclonal/administration & dosage ; Blood-Brain Barrier ; Brain/immunology ; Brain/pathology ; Brain/virology ; Female ; Flow Cytometry/methods ; Immunophenotyping ; Interleukin-12/immunology ; Interleukin-12/metabolism ; Kinetics ; Mice ; Mice, Inbred C57BL ; Microglia/classification ; Microglia/immunology ; Microglia/physiology ; Microglia/virology ; Myeloid Cells/classification ; Myeloid Cells/immunology ; Myeloid Cells/physiology ; Myeloid Cells/virology ; Neuroinflammatory Diseases/immunology ; Neuroinflammatory Diseases/pathology ; Neuroinflammatory Diseases/virology ; Organic Chemicals ; Spatio-Temporal Analysis ; Staining and Labeling ; West Nile Fever/immunology ; West Nile Fever/pathology ; West Nile Fever/virology
Chemical Substances	Antibodies, Monoclonal ; Organic Chemicals ; PLX5622 ; Interleukin-12 (187348-17-0)
Language	English
Publishing date	2021-07-26
Publishing country	England
Document type	Journal Article
ZDB-ID	2156455-3
ISSN	1742-2094 ; 1742-2094
ISSN (online)	1742-2094
ISSN	1742-2094
DOI	10.1186/s12974-021-02214-y
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