Macrophage Antigens and the Effect of a Macrophage Activating Factor, Interferon‐γ

Hogg, Nancy; Selvendran, Yogi; Dougherty, Graeme J.; Allen, Catherine A.

doi:10.1002/9780470720998.ch6

Cited by 6 publications

(1 citation statement)

References 37 publications

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“…An inflammatory response can be induced experimentally by various agents activating microglial cells and astrocytes. The cytokine interferon-γ (IFN-γ), secreted by activated lymphocytes and detected in the brain during the symptomatic phase of MS [ 8 ], can directly activate cells of the macrophage lineage [ 9 - 11 ]. IFN-γ is also able to target oligodendrocytes [ 12 ] and can lead to demyelination after a repeated application [ 13 ].…”

Section: Introductionmentioning

confidence: 99%

Effects of the PPAR-β agonist GW501516 in an in vitro model of brain inflammation and antibody-induced demyelination

Defaux

Zurich

Braissant

et al. 2009

Journal of Neuroinflammation

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BackgroundBrain inflammation plays a central role in numerous brain pathologies, including multiple sclerosis (MS). Microglial cells and astrocytes are the effector cells of neuroinflammation. They can be activated also by agents such as interferon-γ (IFN-γ) and lipopolysaccharide (LPS). Peroxisome proliferator-associated receptor (PPAR) pathways are involved in the control of the inflammatory processes, and PPAR-β seems to play an important role in the regulation of central inflammation. In addition, PPAR-β agonists were shown to have trophic effects on oligodendrocytes in vitro, and to confer partial protection in experimental autoimmune encephalomyelitis (EAE), an animal model of MS. In the present work, a three-dimensional brain cell culture system was used as in vitro model to study antibody-induced demyelination and inflammatory responses. GW 501516, a specific PPAR-β agonist, was examined for its capacity to protect from antibody-mediated demyelination and to prevent inflammatory responses induced by IFN-γ and LPS.MethodsAggregating brain cells cultures were prepared from embryonal rat brain, and used to study the inflammatory responses triggered by IFN-γ and LPS and by antibody-mediated demyelination induced by antibodies directed against myelin-oligodendrocyte glycoprotein (MOG). The effects of GW 501516 on cellular responses were characterized by the quantification of the mRNA expression of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), inducible NO synthase (i-NOS), PPAR-β, PPAR-γ, glial fibrillary acidic protein (GFAP), myelin basic protein (MBP), and high molecular weight neurofilament protein (NF-H). GFAP expression was also examined by immunocytochemistry, and microglial cells were visualized by isolectin B4 (IB4) and ED1 labeling.ResultsGW 501516 decreased the IFN-γ-induced up-regulation of TNF-α and iNOS in accord with the proposed anti-inflammatory effects of this PPAR-β agonist. However, it increased IL-6 m-RNA expression. In demyelinating cultures, reactivity of both microglial cells and astrocytes was observed, while the expression of the inflammatory cytokines and iNOS remained unaffected. Furthermore, GW 501516 did not protect against the demyelination-induced changes in gene expression.ConclusionAlthough GW 501516 showed anti-inflammatory activity, it did not protect against antibody-mediated demyelination. This suggests that the protective effects of PPAR-β agonists observed in vivo can be attributed to their anti-inflammatory properties rather than to a direct protective or trophic effect on oligodendrocytes.

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Section: Introductionmentioning

confidence: 99%

Effects of the PPAR-β agonist GW501516 in an in vitro model of brain inflammation and antibody-induced demyelination

Defaux

Zurich

Braissant

et al. 2009

Journal of Neuroinflammation

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Studies on the Interaction between Murine Resident Bone Marrow Macrophages and Haematopoietic Cells

Crocker

Gordon

1987

Molecular and Cellular Aspects of Erythropoietin and Erythropoiesis

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Comparison of phenotype expression by mononuclear phagocytes within subcutaneous gouty tophi and rheumatoid nodules

Palmer

Hogg²,

Denholm

et al. 1987

Rheumatol Int

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The mononuclear phagocyte infiltrate which occupies the gout tophus has been compared with that of the subcutaneous rheumatoid nodule. In the gout tophus, macrophage migration appears to be at a relatively low level and effectively terminates once these cells have been recruited into the corona. In the nodule the evidence suggests that both macrophage and granulocyte populations continuously migrate towards, and are progressively incorporated into, the necrotic centres. These observations indicate that chemotactic activity in rheumatoid nodules is at a higher level than in gout tophi, or that the rheumatoid mononuclear phagocyte is more responsive to such stimuli.

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Macrophage Antigens and the Effect of a Macrophage Activating Factor, Interferon‐γ

Cited by 6 publications

References 37 publications

Effects of the PPAR-β agonist GW501516 in an in vitro model of brain inflammation and antibody-induced demyelination

Effects of the PPAR-β agonist GW501516 in an in vitro model of brain inflammation and antibody-induced demyelination

Studies on the Interaction between Murine Resident Bone Marrow Macrophages and Haematopoietic Cells

Comparison of phenotype expression by mononuclear phagocytes within subcutaneous gouty tophi and rheumatoid nodules

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