Decreased neuronal CD200 expression in IL-4-deficient mice results in increased neuroinflammation in response to lipopolysaccharide

Lyons, Alan M.; McQuillan, Keith; Deighan, Brian F.; O’Reilly, Julie-Ann; Downer, Eric J.; Murphy, Áine C.; Watson, Melanie B.; Piazza, Alessia; O’Connell, Florence; Griffin, Rebecca J.; Mills, Kingston H. G.; Lynch, Marina A.

doi:10.1016/j.bbi.2009.05.060

Cited by 82 publications

(86 citation statements)

References 38 publications

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“…Loss of CD200 has been associated with evidence of increased inflammatory changes in hippocampal tissue prepared from aged animals as well as LPS-and A␤-treated animals (8,21). In this study, the effects of the TLR4 and TLR2 agonists, LPS and Pam 3 Csk 4 , were assessed on cytokine production in mixed glia prepared from wild type and CD200…”

Section: Resultsmentioning

confidence: 99%

Long Term Potentiation Is Impaired in Membrane Glycoprotein CD200-deficient Mice

Costello¹,

Lyons²,

Denieffe

et al. 2011

Journal of Biological Chemistry

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The membrane glycoprotein CD200 is expressed on several cell types, including neurons, whereas expression of its receptor, CD200R, is restricted principally to cells of the myeloid lineage, including microglia. The interaction between CD200 and CD200R maintains microglia and macrophages in a quiescent state; therefore, CD200-deficient mice express an inflammatory phenotype exhibiting increased macrophage or microglial activation in models of arthritis, encephalitis, and uveoretinitis. Here, we report that lipopolysaccharide (

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Section: Resultsmentioning

confidence: 99%

Long Term Potentiation Is Impaired in Membrane Glycoprotein CD200-deficient Mice

Costello¹,

Lyons²,

Denieffe

et al. 2011

Journal of Biological Chemistry

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132

113

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“…In the past few years, it has been increasingly clear that neuroinflammation negatively impacted on neuronal plasticity and specifically LTP was decreased when microglial activation and/or inflammatory cytokine production were increased in hippocampus (Hall et al 1998;Lyons et al 2009;Lynch 2010). The loss of ovarian oestrogens in postmenopausal women may exacerbate central and peripheral inflammatory responses that occur with normal ageing.…”

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confidence: 99%

Melatonin and oestrogen treatments were able to improve neuroinflammation and apoptotic processes in dentate gyrus of old ovariectomized female rats

Kireev

Vara

Viña

et al. 2014

AGE

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The aim of this study was to determine the outcomes of oestrogen and melatonin treatments following long-term ovarian hormone depletion on neuroinflammation and apoptotic processes in dentate gyrus of hippocampi. Forty-six female Wistar rats of 22 months of age were used. Twelve of them remained intact, and the other 34 were ovariectomized at 12 months of age. Ovariectomized animals were divided into three groups and treated for 10 weeks with oestrogens, melatonin or saline. All rats were killed by decapitation at 24 months of age, and dentate gyri were collected. A group of 2 month-old intact female rats was used as young control. The levels of pro-inflammatory cytokines and heat shock protein 70 (HSP 70) were analysed by ELISA. The expressions of TNFα, IL1β, GFAP, nNOS, iNOS, HO-1, NFκB, Bax, Bad, AIF, Bcl2 and SIRT1 genes were detected by real-time (RT)-PCR. Western blots were used to measure the protein expression of NFκB p65, NFκB p50/105, IκBα, IκBβ, p38 MAPK, MAP-2 and synapsin I. We have assessed the ability of 17β-oestradiol and melatonin administration to downregulate markers of neuroinflammation in the dentate gyrus of ovariectomized female rats. Results indicated that 17β-oestradiol and melatonin treatments were able to significantly decrease expression of pro-inflammatory cytokines, iNOS and HO-1 in the hippocampus when compared to non-treated animals. A similar age-and long-term ovarian hormone depletion-related increase in GFAP was also attenuated after both melatonin and oestradiol treatments. In a similar way to oestradiol, melatonin decreased the activation of p38 MAPK and NFκB pathways. The treatments enhanced the levels of synaptic molecules synapsin I and MAP-2 and have been shown to modulate the pro-antiapoptotic ratio favouring the second and to increase SIRT1 expression. These findings support the potential therapeutic role of melatonin and oestradiol as protective antiinflammatory agents for the central nervous system during menopause.

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“…One factor which increases CD200 expression is IL-4 and, interestingly, a marked reduction in CD200 expression has been reported on neurons prepared from IL-4-deficient mice (Lyons et al, 2009b). Predictably, therefore, co-incubation of mixed glia with neurons prepared from IL-4-deficient mice did not attenuate A -induced production of inflammatory cytokines (Lyons et al, 2009b), contrasting with the effect of neurons prepared from wildtype mice. As highlighted above, endothelial cells express CD200 and, like neurons, incubation of LPS-treated mixed glia with endothelial cells inhibits the LPSinduced release of IL-1 from mixed glia (Figure 2).…”

Section: Cd200-cd200r Interaction Maintains Microglia In a Quiescent mentioning

confidence: 84%

“…Similarly, the A -induced release of IL-1 , IL-6 and TNFα from mixed glia is inhibited when cells are co-cultured with neurons and this effect of neurons is also inhibited by the presence of a blocking anti-CD200 antibody (Lyons et al, 2007a). One factor which increases CD200 expression is IL-4 and, interestingly, a marked reduction in CD200 expression has been reported on neurons prepared from IL-4-deficient mice (Lyons et al, 2009b). Predictably, therefore, co-incubation of mixed glia with neurons prepared from IL-4-deficient mice did not attenuate A -induced production of inflammatory cytokines (Lyons et al, 2009b), contrasting with the effect of neurons prepared from wildtype mice.…”

Section: Cd200-cd200r Interaction Maintains Microglia In a Quiescent mentioning

confidence: 97%

“…Evidence from this laboratory has revealed that co-culture of neurons with mixed glia inhibited LPSinduced increases in release of IL-1 , IL-6 and TNFα. The effect of neurons was blocked when the incubation was carried out in the presence of a blocking anti-CD200 antibody (Lyons et al, 2009b) pinpointing a role for CD200 in modulating cytokine release. Similarly, the A -induced release of IL-1 , IL-6 and TNFα from mixed glia is inhibited when cells are co-cultured with neurons and this effect of neurons is also inhibited by the presence of a blocking anti-CD200 antibody (Lyons et al, 2007a).…”

Section: Cd200-cd200r Interaction Maintains Microglia In a Quiescent mentioning

confidence: 99%

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Analysis of the Impact of CD200 on Neurodegenerative Diseases

Miller¹,

Deighan²,

Downer³

et al. 2011

Neurodegenerative Diseases - Processes, Prevention, Protection and Monitoring

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Decreased neuronal CD200 expression in IL-4-deficient mice results in increased neuroinflammation in response to lipopolysaccharide

Cited by 82 publications

References 38 publications

Long Term Potentiation Is Impaired in Membrane Glycoprotein CD200-deficient Mice

Long Term Potentiation Is Impaired in Membrane Glycoprotein CD200-deficient Mice

Melatonin and oestrogen treatments were able to improve neuroinflammation and apoptotic processes in dentate gyrus of old ovariectomized female rats

Analysis of the Impact of CD200 on Neurodegenerative Diseases

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