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  1. Article: Nanomodulation of Macrophages in Multiple Sclerosis.

    Nally, Frances K / De Santi, Chiara / McCoy, Claire E

    Cells

    2019  Volume 8, Issue 6

    Abstract: Multiple Sclerosis (MS) is a chronic demyelinating autoimmune disease primarily affecting young adults. Despite an unclear causal factor, symptoms and pathology arise from the infiltration of peripheral immune cells across the blood brain barrier. ... ...

    Abstract Multiple Sclerosis (MS) is a chronic demyelinating autoimmune disease primarily affecting young adults. Despite an unclear causal factor, symptoms and pathology arise from the infiltration of peripheral immune cells across the blood brain barrier. Accounting for the largest fraction of this infiltrate, macrophages are functionally heterogeneous innate immune cells capable of adopting either a pro or an anti-inflammatory phenotype, a phenomenon dependent upon cytokine milieu in the CNS. This functional plasticity is of key relevance in MS, where the pro-inflammatory state dominates the early stage, instructing demyelination and axonal loss while the later anti-inflammatory state holds a key role in promoting tissue repair and regeneration in later remission. This review highlights a potential therapeutic benefit of modulating macrophage polarisation to harness the anti-inflammatory and reparative state in MS. Here, we outline the role of macrophages in MS and look at the role of current FDA approved therapeutics in macrophage polarisation. Moreover, we explore the potential of particulate carriers as a novel strategy to manipulate polarisation states in macrophages, whilst examining how optimising macrophage uptake via nanoparticle size and functionalisation could offer a novel therapeutic approach for MS.
    MeSH term(s) Central Nervous System/immunology ; Central Nervous System/metabolism ; Drug Carriers/chemistry ; Humans ; Immunologic Factors/chemistry ; Immunologic Factors/therapeutic use ; Immunosuppressive Agents/chemistry ; Immunosuppressive Agents/therapeutic use ; Macrophages/cytology ; Macrophages/immunology ; Macrophages/metabolism ; Multiple Sclerosis/drug therapy ; Multiple Sclerosis/immunology ; Multiple Sclerosis/pathology ; Nanoparticles/chemistry
    Chemical Substances Drug Carriers ; Immunologic Factors ; Immunosuppressive Agents
    Language English
    Publishing date 2019-06-05
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2661518-6
    ISSN 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells8060543
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Enhancing arginase 2 expression using target site blockers as a strategy to modulate macrophage phenotype.

    De Santi, Chiara / Nally, Frances K / Afzal, Remsha / Duffy, Conor P / Fitzsimons, Stephen / Annett, Stephanie L / Robson, Tracy / Dowling, Jennifer K / Cryan, Sally-Ann / McCoy, Claire E

    Molecular therapy. Nucleic acids

    2022  Volume 29, Page(s) 643–655

    Abstract: Macrophages are plastic cells playing a crucial role in innate immunity. While fundamental in responding to infections, when persistently maintained in a pro-inflammatory state they can initiate and sustain inflammatory diseases. Therefore, a strategy ... ...

    Abstract Macrophages are plastic cells playing a crucial role in innate immunity. While fundamental in responding to infections, when persistently maintained in a pro-inflammatory state they can initiate and sustain inflammatory diseases. Therefore, a strategy that reprograms pro-inflammatory macrophages toward an anti-inflammatory phenotype could hold therapeutic potential in that context. We have recently shown that arginase 2 (Arg2), a mitochondrial enzyme involved in arginine metabolism, promotes the resolution of inflammation in macrophages and it is targeted by miR-155. Here, we designed and tested a target site blocker (TSB) that specifically interferes and blocks the interaction between miR-155 and
    Language English
    Publishing date 2022-08-04
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2662631-7
    ISSN 2162-2531
    ISSN 2162-2531
    DOI 10.1016/j.omtn.2022.08.004
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Mitochondrial arginase-2 is essential for IL-10 metabolic reprogramming of inflammatory macrophages.

    Dowling, Jennifer K / Afzal, Remsha / Gearing, Linden J / Cervantes-Silva, Mariana P / Annett, Stephanie / Davis, Gavin M / De Santi, Chiara / Assmann, Nadine / Dettmer, Katja / Gough, Daniel J / Bantug, Glenn R / Hamid, Fidinny I / Nally, Frances K / Duffy, Conor P / Gorman, Aoife L / Liddicoat, Alex M / Lavelle, Ed C / Hess, Christoph / Oefner, Peter J /
    Finlay, David K / Davey, Gavin P / Robson, Tracy / Curtis, Annie M / Hertzog, Paul J / Williams, Bryan R G / McCoy, Claire E

    Nature communications

    2021  Volume 12, Issue 1, Page(s) 1460

    Abstract: Mitochondria are important regulators of macrophage polarisation. Here, we show that arginase-2 (Arg2) is a microRNA-155 (miR-155) and interleukin-10 (IL-10) regulated protein localized at the mitochondria in inflammatory macrophages, and is critical for ...

    Abstract Mitochondria are important regulators of macrophage polarisation. Here, we show that arginase-2 (Arg2) is a microRNA-155 (miR-155) and interleukin-10 (IL-10) regulated protein localized at the mitochondria in inflammatory macrophages, and is critical for IL-10-induced modulation of mitochondrial dynamics and oxidative respiration. Mechanistically, the catalytic activity and presence of Arg2 at the mitochondria is crucial for oxidative phosphorylation. We further show that Arg2 mediates this process by increasing the activity of complex II (succinate dehydrogenase). Moreover, Arg2 is essential for IL-10-mediated downregulation of the inflammatory mediators succinate, hypoxia inducible factor 1α (HIF-1α) and IL-1β in vitro. Accordingly, HIF-1α and IL-1β are highly expressed in an LPS-induced in vivo model of acute inflammation using Arg2
    MeSH term(s) Animals ; Arginase/genetics ; Arginase/metabolism ; Down-Regulation ; Female ; Interleukin-10/metabolism ; Interleukin-1beta/metabolism ; Macrophages/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout/genetics ; Mitochondria/enzymology ; Mitochondria/metabolism ; Succinate Dehydrogenase/metabolism
    Chemical Substances Interleukin-1beta ; Interleukin-10 (130068-27-8) ; Succinate Dehydrogenase (EC 1.3.99.1) ; Arg2 protein, mouse (EC 3.5.3.1) ; Arginase (EC 3.5.3.1)
    Language English
    Publishing date 2021-03-05
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-021-21617-2
    Database MEDical Literature Analysis and Retrieval System OnLINE

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