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  1. Article ; Online: Cell death by phagocytosis.

    Brown, Guy C

    Nature reviews. Immunology

    2023  Volume 24, Issue 2, Page(s) 91–102

    Abstract: Cells can die as a consequence of being phagocytosed by other cells - a form of cell death that has been called phagotrophy, cell cannibalism, programmed cell removal and primary phagocytosis. However, these are all different manifestations of cell death ...

    Abstract Cells can die as a consequence of being phagocytosed by other cells - a form of cell death that has been called phagotrophy, cell cannibalism, programmed cell removal and primary phagocytosis. However, these are all different manifestations of cell death by phagocytosis (termed 'phagoptosis' for short). The engulfed cells die as a result of cytotoxic oxidants, peptides and degradative enzymes within acidic phagolysosomes. Cell death by phagocytosis was discovered by Metchnikov in the 1880s, but was neglected until recently. It is now known to contribute to developmental cell death in nematodes, Drosophila and mammals, and is central to innate and adaptive immunity against pathogens. Cell death by phagocytosis mediates physiological turnover of erythrocytes and other leucocytes, making it the most abundant form of cell death in the mammalian body. Immunity against cancer is also partly mediated by macrophage phagocytosis of cancer cells, but cancer cells can also phagocytose host cells and other cancer cells in order to survive. Recent evidence indicates neurodegeneration and other neuropathologies can be mediated by microglial phagocytosis of stressed neurons. Thus, despite cell death by phagocytosis being poorly recognized, it is one of the oldest, commonest and most important forms of cell death.
    MeSH term(s) Animals ; Humans ; Cell Death/physiology ; Phagocytosis/physiology ; Microglia/metabolism ; Macrophages ; Neurons ; Mammals
    Language English
    Publishing date 2023-08-21
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2062776-2
    ISSN 1474-1741 ; 1474-1733
    ISSN (online) 1474-1741
    ISSN 1474-1733
    DOI 10.1038/s41577-023-00921-6
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5565: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)
    Zs.MG 34: Show issues

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  2. Book: Mitochondrial function

    Brown, Guy C.

    (Essays in biochemistry ; 47)

    2010  

    Author's details ed. by G. C. Brown
    Series title Essays in biochemistry ; 47
    Collection
    Language English
    Size XIX, 155 S. : Ill., graph. Darst.
    Publisher Portland Press
    Publishing place London
    Publishing country Great Britain
    Document type Book
    HBZ-ID HT016475043
    ISBN 978-1-85578-178-8 ; 1-85578-178-6
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    Zs A 12 -47- not available for loan Zeitschriften-Lesesaal

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  3. Article ; Online: The endotoxin hypothesis of Alzheimer's disease.

    Brown, Guy C / Heneka, Michael T

    Molecular neurodegeneration

    2024  Volume 19, Issue 1, Page(s) 30

    Abstract: Lipopolysaccharide (LPS) constitutes much of the surface of Gram-negative bacteria, and if LPS enters the human body or brain can induce inflammation and act as an endotoxin. We outline the hypothesis here that LPS may contribute to the pathophysiology ... ...

    Abstract Lipopolysaccharide (LPS) constitutes much of the surface of Gram-negative bacteria, and if LPS enters the human body or brain can induce inflammation and act as an endotoxin. We outline the hypothesis here that LPS may contribute to the pathophysiology of Alzheimer's disease (AD) via peripheral infections or gut dysfunction elevating LPS levels in blood and brain, which promotes: amyloid pathology, tau pathology and microglial activation, contributing to the neurodegeneration of AD. The evidence supporting this hypothesis includes: i) blood and brain levels of LPS are elevated in AD patients, ii) AD risk factors increase LPS levels or response, iii) LPS induces Aβ expression, aggregation, inflammation and neurotoxicity, iv) LPS induces TAU phosphorylation, aggregation and spreading, v) LPS induces microglial priming, activation and neurotoxicity, and vi) blood LPS induces loss of synapses, neurons and memory in AD mouse models, and cognitive dysfunction in humans. However, to test the hypothesis, it is necessary to test whether reducing blood LPS reduces AD risk or progression. If the LPS endotoxin hypothesis is correct, then treatments might include: reducing infections, changing gut microbiome, reducing leaky gut, decreasing blood LPS, or blocking LPS response.
    MeSH term(s) Mice ; Animals ; Humans ; Alzheimer Disease/metabolism ; Endotoxins/toxicity ; Endotoxins/metabolism ; Lipopolysaccharides ; Microglia/metabolism ; Inflammation/metabolism ; Amyloid beta-Peptides/metabolism
    Chemical Substances Endotoxins ; Lipopolysaccharides ; Amyloid beta-Peptides
    Language English
    Publishing date 2024-04-01
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2244557-2
    ISSN 1750-1326 ; 1750-1326
    ISSN (online) 1750-1326
    ISSN 1750-1326
    DOI 10.1186/s13024-024-00722-y
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Book: The living end

    Brown, Guy C.

    the future of death, aging and immortality

    2008  

    Author's details Guy Brown
    Keywords Death ; Attitude to Death ; Aging / physiology
    Language English
    Size VI, 278 S. : graph. Darst.
    Publisher Macmillan
    Publishing place London u.a.
    Publishing country Great Britain
    Document type Book
    Note Hier auch später erschienene, unveränderte Nachdrucke
    HBZ-ID HT015615528
    ISBN 978-0-2305-1757-8 ; 0-2305-1757-9 ; 978-1-349-95369-1 ; 1-349-95369-5
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    2008 A 4271 order for loan Magazin

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  5. Article ; Online: Neuronal Loss after Stroke Due to Microglial Phagocytosis of Stressed Neurons.

    Brown, Guy C

    International journal of molecular sciences

    2021  Volume 22, Issue 24

    Abstract: After stroke, there is a rapid necrosis of all cells in the infarct, followed by a delayed loss of neurons both in brain areas surrounding the infarct, known as 'selective neuronal loss', and in brain areas remote from, but connected to, the infarct, ... ...

    Abstract After stroke, there is a rapid necrosis of all cells in the infarct, followed by a delayed loss of neurons both in brain areas surrounding the infarct, known as 'selective neuronal loss', and in brain areas remote from, but connected to, the infarct, known as 'secondary neurodegeneration'. Here we review evidence indicating that this delayed loss of neurons after stroke is mediated by the microglial phagocytosis of stressed neurons. After a stroke, neurons are stressed by ongoing ischemia, excitotoxicity and/or inflammation and are known to: (i) release "find-me" signals such as ATP, (ii) expose "eat-me" signals such as phosphatidylserine, and (iii) bind to opsonins, such as complement components C1q and C3b, inducing microglia to phagocytose such neurons. Blocking these factors on neurons, or their phagocytic receptors on microglia, can prevent delayed neuronal loss and behavioral deficits in rodent models of ischemic stroke. Phagocytic receptors on microglia may be attractive treatment targets to prevent delayed neuronal loss after stroke due to the microglial phagocytosis of stressed neurons.
    MeSH term(s) Animals ; Brain/metabolism ; Brain/pathology ; Humans ; Inflammation/metabolism ; Inflammation/pathology ; Microglia/metabolism ; Microglia/pathology ; Neurons/metabolism ; Neurons/pathology ; Phagocytosis ; Stroke/metabolism ; Stroke/pathology
    Language English
    Publishing date 2021-12-14
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms222413442
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  6. Article: Activated microglia release β-galactosidase that promotes inflammatory neurodegeneration.

    Kitchener, Emily J A / Dundee, Jacob M / Brown, Guy C

    Frontiers in aging neuroscience

    2024  Volume 15, Page(s) 1327756

    Abstract: Beta (β)-galactosidase is a lysosomal enzyme that removes terminal galactose residues from glycolipids and glycoproteins. It is upregulated in, and used as a marker for, senescent cells. Microglia are brain macrophages implicated in neurodegeneration, ... ...

    Abstract Beta (β)-galactosidase is a lysosomal enzyme that removes terminal galactose residues from glycolipids and glycoproteins. It is upregulated in, and used as a marker for, senescent cells. Microglia are brain macrophages implicated in neurodegeneration, and can upregulate β-galactosidase when senescent. We find that inflammatory activation of microglia induced by lipopolysaccharide results in translocation of β-galactosidase to the cell surface and release into the medium. Similarly, microglia in aged mouse brains appear to have more β-galactosidase on their surface. Addition of β-galactosidase to neuronal-glial cultures causes microglial activation and neuronal loss mediated by microglia. Inhibition of β-galactosidase in neuronal-glial cultures reduces inflammation and neuronal loss induced by lipopolysaccharide. Thus, activated microglia release β-galactosidase that promotes microglial-mediated neurodegeneration which is prevented by inhibition of β-galactosidase.
    Language English
    Publishing date 2024-01-12
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2558898-9
    ISSN 1663-4365
    ISSN 1663-4365
    DOI 10.3389/fnagi.2023.1327756
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  7. Article ; Online: LRPAP1 is released from activated microglia and inhibits microglial phagocytosis and amyloid beta aggregation.

    Reid, Kyle M / Brown, Guy C

    Frontiers in immunology

    2023  Volume 14, Page(s) 1286474

    Abstract: Low-density lipoprotein receptor-related protein-associated protein 1 (LRPAP1), also known as receptor associated protein (RAP), is an endoplasmic reticulum (ER) chaperone and inhibitor of LDL receptor related protein 1 (LRP1) and related receptors. ... ...

    Abstract Low-density lipoprotein receptor-related protein-associated protein 1 (LRPAP1), also known as receptor associated protein (RAP), is an endoplasmic reticulum (ER) chaperone and inhibitor of LDL receptor related protein 1 (LRP1) and related receptors. These receptors have dozens of physiological ligands and cell functions, but it is not known whether cells release LRPAP1 physiologically at levels that regulate these receptors and cell functions. We used mouse BV-2 and human CHME3 microglial cell lines, and found that microglia released nanomolar levels of LRPAP1 when inflammatory activated by lipopolysaccharide or when ER stressed by tunicamycin. LRPAP1 was found on the surface of live activated and non-activated microglia, and anti-LRPAP1 antibodies induced internalization. Addition of 10 nM LRPAP1 inhibited microglial phagocytosis of isolated synapses and cells, and the uptake of Aβ. LRPAP1 also inhibited Aβ aggregation
    MeSH term(s) Animals ; Humans ; Mice ; Amyloid beta-Peptides/metabolism ; Carrier Proteins/metabolism ; Cell Line ; Cells, Cultured ; Microglia ; Phagocytosis ; LDL-Receptor Related Protein-Associated Protein/metabolism
    Chemical Substances Amyloid beta-Peptides ; Carrier Proteins ; LDL-Receptor Related Protein-Associated Protein
    Language English
    Publishing date 2023-11-16
    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.2023.1286474
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Neuronal Loss after Stroke Due to Microglial Phagocytosis of Stressed Neurons

    Guy C. Brown

    International Journal of Molecular Sciences, Vol 22, Iss 13442, p

    2021  Volume 13442

    Abstract: After stroke, there is a rapid necrosis of all cells in the infarct, followed by a delayed loss of neurons both in brain areas surrounding the infarct, known as ‘selective neuronal loss’, and in brain areas remote from, but connected to, the infarct, ... ...

    Abstract After stroke, there is a rapid necrosis of all cells in the infarct, followed by a delayed loss of neurons both in brain areas surrounding the infarct, known as ‘selective neuronal loss’, and in brain areas remote from, but connected to, the infarct, known as ‘secondary neurodegeneration’. Here we review evidence indicating that this delayed loss of neurons after stroke is mediated by the microglial phagocytosis of stressed neurons. After a stroke, neurons are stressed by ongoing ischemia, excitotoxicity and/or inflammation and are known to: (i) release “find-me” signals such as ATP, (ii) expose “eat-me” signals such as phosphatidylserine, and (iii) bind to opsonins, such as complement components C1q and C3b, inducing microglia to phagocytose such neurons. Blocking these factors on neurons, or their phagocytic receptors on microglia, can prevent delayed neuronal loss and behavioral deficits in rodent models of ischemic stroke. Phagocytic receptors on microglia may be attractive treatment targets to prevent delayed neuronal loss after stroke due to the microglial phagocytosis of stressed neurons.
    Keywords stroke ; cell death ; neuronal death ; delayed neuronal death ; selective neuronal loss ; secondary neurodegeneration ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Subject code 590
    Language English
    Publishing date 2021-12-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  9. Article ; Online: Knockout of the P2Y

    Milde, Stefan / Brown, Guy C

    International journal of molecular sciences

    2022  Volume 23, Issue 4

    Abstract: After stroke, there is a delayed neuronal loss in brain areas surrounding the infarct, which may in part be mediated by microglial phagocytosis of stressed neurons. Microglial phagocytosis of stressed or damaged neurons can be mediated by UDP released ... ...

    Abstract After stroke, there is a delayed neuronal loss in brain areas surrounding the infarct, which may in part be mediated by microglial phagocytosis of stressed neurons. Microglial phagocytosis of stressed or damaged neurons can be mediated by UDP released from stressed neurons activating the P2Y
    MeSH term(s) Animals ; Brain/metabolism ; Brain/pathology ; Brain Infarction/metabolism ; Brain Infarction/pathology ; Brain Ischemia/metabolism ; Brain Ischemia/pathology ; Cells, Cultured ; Female ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Microglia/metabolism ; Microglia/pathology ; Neurons/metabolism ; Neurons/pathology ; Phagocytosis/physiology ; Receptors, Purinergic P2/metabolism ; Stroke/metabolism ; Stroke/pathology
    Chemical Substances Receptors, Purinergic P2 ; purinoceptor P2Y6
    Language English
    Publishing date 2022-02-19
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms23042304
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article: Neu1 Is Released From Activated Microglia, Stimulating Microglial Phagocytosis and Sensitizing Neurons to Glutamate.

    Allendorf, David H / Brown, Guy C

    Frontiers in cellular neuroscience

    2022  Volume 16, Page(s) 917884

    Abstract: Neuraminidase 1 (Neu1) hydrolyses terminal sialic acid residues from glycoproteins and glycolipids, and is normally located in lysosomes, but can be released onto the surface of activated myeloid cells and microglia. We report that endotoxin/ ... ...

    Abstract Neuraminidase 1 (Neu1) hydrolyses terminal sialic acid residues from glycoproteins and glycolipids, and is normally located in lysosomes, but can be released onto the surface of activated myeloid cells and microglia. We report that endotoxin/lipopolysaccharide-activated microglia released Neu1 into culture medium, and knockdown of Neu1 in microglia reduced both Neu1 protein and neuraminidase activity in the culture medium. Release of Neu1 was reduced by inhibitors of lysosomal exocytosis, and accompanied by other lysosomal proteins, including protective protein/cathepsin A, known to keep Neu1 active. Extracellular neuraminidase or over-expression of Neu1 increased microglial phagocytosis, while knockdown of Neu1 decreased phagocytosis. Microglial activation caused desialylation of microglial phagocytic receptors Trem2 and MerTK, and increased binding to Trem2 ligand galectin-3. Culture media from activated microglia contained Neu1, and when incubated with neurons induced their desialylation, and increased the neuronal death induced by low levels of glutamate. Direct desialylation of neurons by adding sialidase or inhibiting sialyltransferases also increased glutamate-induced neuronal death. We conclude that activated microglia can release active Neu1, possibly by lysosomal exocytosis, and this can both increase microglial phagocytosis and sensitize neurons to glutamate, thus potentiating neuronal death.
    Language English
    Publishing date 2022-05-26
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2452963-1
    ISSN 1662-5102
    ISSN 1662-5102
    DOI 10.3389/fncel.2022.917884
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