Leukemia inhibitory factor modulates production of inflammatory mediators and myelin phagocytosis by macrophages

Hendriks, Jerome J. A.; Slaets, Helena; Carmans, Sofie; Vries, Helga E. de; Dijkstra, Christine D.; Stinissen, Piet; Hellings, Niels

doi:10.1016/j.jneuroim.2008.07.015

Cited by 56 publications

(49 citation statements)

References 44 publications

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“…On the other hand, IL-6 is reported to promote survival of oligodendrocytes in vitro and in vivo (Louis et al, 1993). LIF is reported to promote maturation of oligodendrocytes (Ishibashi et al, 2006) and enhance myelin clearance (Hendriks et al, 2008). Moreover, IL-6 and LIF released by microglia promote the astrocytic differentiation of neural stem/progenitor cells (Nakanishi et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

Time-dependent changes in proinflammatory and neurotrophic responses of microglia and astrocytes in a rat model of osmotic demyelination syndrome

Iwama

Sugimura

Suzuki

et al. 2010

Glia

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Osmotic demyelination syndrome (ODS) is a serious demyelinating disease in the central nervous system usually caused by rapid correction of hyponatremia. In an animal model of ODS, we previously reported microglial accumulation expressing proinflammatory cytokines. Microglia and astrocytes secreting proinflammatory cytokines and neurotrophic factors are reported to be involved in the pathogenesis of demyelinative diseases. Therefore, to clarify the role of microglial and astrocytic function in ODS, we examined the time-dependent changes in distribution, morphology, proliferation, and mRNA/protein expression of proinflammatory cytokines, neurotrophic factors, and matrix metalloproteinase (MMP) in microglia and astrocytes 2 days (early phase) and 5 days (late phase) after the rapid correction of hyponatremia in ODS rats. The number of microglia time dependently increased at demyelinative lesion sites, proliferated, and expressed tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, inducible nitric oxide synthase, and MMP2, 9, and 12 at the early phase. Microglia also expressed leukemia inhibitory factor (a neurotrophic factor) and phagocytosed myelin debris at the late phase. The number of astrocytes time dependently increased around demyelinative lesions, extended processes to lesions, proliferated, and expressed nerve growth factor and glial cell line-derived neurotrophic factor at the late phase. Moreover, treatment with infliximab, a monoclonal antibody against TNF-α, significantly attenuated neurological impairments. Our results suggest that the role of microglia in ODS is time dependently shifted from detrimental to protective and that astrocytes play a protective role at the late phase. Modulation of excessive proinflammatory responses in microglia during the early phase after rapid correction may represent a therapeutic target for ODS.

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Section: Discussionmentioning

confidence: 99%

Time-dependent changes in proinflammatory and neurotrophic responses of microglia and astrocytes in a rat model of osmotic demyelination syndrome

Iwama

Sugimura

Suzuki

et al. 2010

Glia

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“…Supernatant was discarded and labeled myelin was further resuspended in sterile PBS to a final concentration of 1mg/ml and stored at -20ºC (Hendriks et al 2008, van der Laan et al 1996). …”

Section: Myelin Isolation and Labellingmentioning

confidence: 99%

“…Cells were detached by adding PBS/5 mM EDTA for 15 min at 37ºC and cell fluorescence was determined by flow cytometry using a FACScalibur cytometer. Intensity and percentage of positive cells were used to quatify Dil-labeled myelin uptake after treatments (Hendriks et al 2008).…”

Section: Myelin Phagocytosis Assaymentioning

confidence: 99%

Mechanisms Involved in the Remyelinating Effect of Sildenafil

Díaz-Lucena

Gutièrrez‐Mecinas

Moreno

et al. 2017

J Neuroimmune Pharmacol

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ADVERTIMENT. Lʼaccés als continguts dʼaquesta tesi doctoral i la seva utilització ha de respectar els drets de la persona autora. Pot ser utilitzada per a consulta o estudi personal, així com en activitats o materials dʼinvestigació i docència en els termes establerts a lʼart. 32 del Text Refós de la Llei de Propietat Intel·lectual (RDL 1/1996). Per altres utilitzacions es requereix lʼautorització prèvia i expressa de la persona autora. En qualsevol cas, en la utilització dels seus continguts caldrà indicar de forma clara el nom i cognoms de la persona autora i el títol de la tesi doctoral. No sʼautoritza la seva reproducció o altres formes dʼexplotació efectuades amb finalitats de lucre ni la seva comunicació pública des dʼun lloc aliè al servei TDX. Tampoc sʼautoritza la presentació del seu contingut en una finestra o marc aliè a TDX (framing). Aquesta reserva de drets afecta tant als continguts de la tesi com als seus resums i índexs.ADVERTENCIA. El acceso a los contenidos de esta tesis doctoral y su utilización debe respetar los derechos de la persona autora. Puede ser utilizada para consulta o estudio personal, así como en actividades o materiales de investigación y docencia en los términos establecidos en el art. 32 del Texto Refundido de la Ley de Propiedad Intelectual (RDL 1/1996). Para otros usos se requiere la autorización previa y expresa de la persona autora. En cualquier caso, en la utilización de sus contenidos se deberá indicar de forma clara el nombre y apellidos de la persona autora y el título de la tesis doctoral. No se autoriza su reproducción u otras formas de explotación efectuadas con fines lucrativos ni su comunicación pública desde un sitio ajeno al servicio TDR. Tampoco se autoriza la presentación de su contenido en una ventana o marco ajeno a TDR (framing). Esta reserva de derechos afecta tanto al contenido de la tesis como a sus resúmenes e índices.WARNING.

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“…IL-10) or both proand anti-inflammatory activities (e.g. LIF) (Smith et al 1998;Hendriks et al 2008). …”

Section: Regulation Of Phagocytic Activity Of Microgliamentioning

confidence: 99%

“…Expression of IGF-1 has been shown to be induced in microglia in response to leukemia inhibitory factor (LIF) in an in vivo model of spinal cord injury (Kerr and Patterson 2005). The LIF is a neuropoietic cytokine that belongs to the IL-6 family that has also been shown to inhibit the production of oxygen radicals and TNF-a by macrophages (Hendriks et al 2008) and which is induced in EAE and cuprizone models of inflammatory demyelination. Previous research has demonstrated that exogenous LIF increases oligodendrocyte survival both during EAE and after cuprizone challenge, independent of peripheral immune effects (Butzkueven et al 2002;Butzkueven et al 2006;Marriott et al 2008).…”

Section: Cytokines Exhibiting Neuroprotective/trophic Effectsmentioning

confidence: 99%

Role of Cytokines as Mediators and Regulators of Microglial Activity in Inflammatory Demyelination of the CNS

2010

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As the resident innate immune cells of the central nervous system (CNS), microglia fulfil a critical role in maintaining tissue homeostasis and in directing and eliciting molecular responses to CNS damage. The human disease Multiple Sclerosis and animal models of inflammatory demyelination are characterized by a complex interplay between degenerative and regenerative processes, many of which are regulated and mediated by microglia. Cellular communication between microglia and other neural and immune cells is controlled to a large extent by the activity of cytokines. Here we review the role of cytokines as mediators and regulators of microglial activity in inflammatory demyelination, highlighting their importance in potentiating cell damage, promoting neuroprotection and enhancing cellular repair in a context-dependent manner.

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Leukemia inhibitory factor modulates production of inflammatory mediators and myelin phagocytosis by macrophages

Cited by 56 publications

References 44 publications

Time-dependent changes in proinflammatory and neurotrophic responses of microglia and astrocytes in a rat model of osmotic demyelination syndrome

Time-dependent changes in proinflammatory and neurotrophic responses of microglia and astrocytes in a rat model of osmotic demyelination syndrome

Mechanisms Involved in the Remyelinating Effect of Sildenafil

Role of Cytokines as Mediators and Regulators of Microglial Activity in Inflammatory Demyelination of the CNS

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