Interleukin-1β-Induced Changes in Blood–Brain Barrier Permeability, Apparent Diffusion Coefficient, and Cerebral Blood Volume in the Rat Brain: A Magnetic Resonance Study

Blamire, Andrew M.; Anthony, Daniel C.; Rajagopalan, B; Sibson, Nicola R.; Perry, V. Hugh; Styles, Peter

doi:10.1523/jneurosci.20-21-08153.2000

Cited by 208 publications

(161 citation statements)

References 56 publications

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“…The mechanism underlying the increase in rCBV is unclear but may reflect, at least in part, (1) reactivation of metabolically active leukocytes, (2) local produc- tion of the vasodilator nitric oxide (Willenborg et al, 1999), or (3) increased expression of local cytokines. We have shown previously that injection of IL-1␤ into the rat brain results in an acute increase in rCBV (Blamire et al, 2000). It is also known that peripheral injection of LPS induces IL-1␤ expression in both the periphery and the brain (Zetterström et al, 1998;McColl et al, 2007).…”

Section: Discussionmentioning

confidence: 95%

Systemic Inflammatory Response Reactivates Immune-Mediated Lesions in Rat Brain

Serres¹,

Anthony²,

Jiang³

et al. 2009

J. Neurosci.

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107

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The potential association between microbial infection and reactivation of a multiple sclerosis (MS) lesion is an important issue that remains unresolved, primarily because of the absence of suitable animal models and imaging techniques. Here, we have evaluated this question in an empirical manner using immunohistochemistry and magnetic resonance imaging (MRI), before and after the induction of a systemic inflammatory response in two distinct models of MS. In a pattern-II-type focal myelin oligodendrocyte glycoproteinexperimental autoimmune encephalomyelitis model, systemic endotoxin injection caused an increase in regional cerebral blood volume (rCBV) around the lesion site after 6 h, together with a reduction in the magnetization transfer ratio of the lesioned corpus callosum. These changes were followed by an increase in the diffusion of tissue water within the lesion 24 h after endotoxin challenge and new leukocyte recruitment as revealed both immunohistochemically and by MRI tracking of ultrasmall superparamagnetic iron oxidelabeled macrophages. Importantly, we detected in vivo expression of E-and P-selectin in quiescent lesions by MRI-detectable glyconanoparticles conjugated to sialyl Lewis X . This finding may explain, at least in part, the ability of quiescent MS lesions to rapidly reinitiate the cell recruitment processes. In a pattern-I-type delayed-type hypersensitivity response model, a similar effect of endotoxin challenge on rCBV was observed, together with delayed breakdown of the blood-brain barrier, showing that systemic infection can alter the pathogenesis of MS-like lesions regardless of lesion etiology. These findings will have important implications for the management and monitoring of individuals with MS.

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Section: Discussionmentioning

confidence: 95%

Systemic Inflammatory Response Reactivates Immune-Mediated Lesions in Rat Brain

Serres¹,

Anthony²,

Jiang³

et al. 2009

J. Neurosci.

Self Cite

107

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“…Besides MCP1, many other cytokines, including interleukin (IL)-1, IL-4, IL-8, IL-10, IL-13, tumor necrosis factor (TNF)-a and interferon (IFN)- (Ahdieh et al, 2001;Blamire et al, 2000;Coyne et al, 2002;Paul et al, 2003;Ross and Joyner, 1997;Wojciak-Stothard et al, 1998;Yang et al, 1999;Youakim and Ahdieh, 1999), have been shown to change the structure of tight junctions and promote the formation of stress fibers in epithelial and endothelial cells. Whether these molecules induce BBB compromise using the same signaling pathways is not clear; however, on the basis of the conserved function and high expression level of ERM proteins in epithelial and endothelial cells, we would assume the same signaling pathways are activated upon the cytokine treatment.…”

Section: Discussionmentioning

confidence: 99%

Truncation of monocyte chemoattractant protein 1 by plasmin promotes blood–brain barrier disruption

Yao

Tsirka

2011

Journal of Cell Science

102

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SummaryPrevious studies have shown that plasmin cleaves monocyte chemoattractant protein 1 (MCP1; officially known as C-C motif chemokine 2, CCL2) at K104, and this cleavage enhances its chemotactic potency significantly. Accumulating evidence reveals that MCP1 also disrupts the integrity of the blood-brain barrier (BBB). Here, we show that K104Stop-MCP1, truncated at the K104 where plasmin would normally cleave, is more efficient than the full-length protein (FL-MCP1) in compromising the integrity of the BBB in in vitro and in vivo models. K104Stop-MCP1 increases the permeability of BBB in both wild-type mice and mice deficient for tissue plasminogen activator (tPA), which converts plasminogen into active plasmin, suggesting that plasmin-mediated truncation of MCP1 plays an important role in BBB compromise. Furthermore, we show that the mechanisms underlying MCP1-induced BBB disruption involve redistribution of tight junction proteins (occludin and ZO-1) and reorganization of the actin cytoskeleton. Finally, we show that the redistribution of ZO-1 is mediated by phosphorylation of ezrin-radixin-moesin (ERM) proteins. These findings identify plasmin as a key signaling molecule in the regulation of BBB integrity and suggest that plasmin inhibitors might be used to modulate diseases accompanied by BBB compromise.

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“…To address the potential role of these inflammatory processes in the opening of the BBB (Blamire et al, 2000) we aimed to mimic the remote Gf accumulation after PT by systemic LPS application. Groups of three naive rats received LPS (0.5 mg/kg body weight) intraperitoneally and Gf 1 or 48 h thereafter i.v., and underwent MRI at 24 or 72 h, respectively.…”

Section: N -Methyl-d -Aspartate-receptor Blockage and Lipopolysaccharmentioning

confidence: 99%

Transient Widespread Blood—Brain Barrier Alterations after Cerebral Photothrombosis as Revealed by Gadofluorine M-Enhanced Magnetic Resonance Imaging

Stoll

Kleinschnitz

Meuth

et al. 2008

J Cereb Blood Flow Metab

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Magnetic resonance imaging (MRI) is a powerful tool to assess brain lesions, but currently available contrast agents are limited in the assessment of cellular and functional alterations. By use of the novel MRI contrast agent gadofluorine M (Gf) we report on imaging of transient and widespread changes of blood-brain barrier (BBB) properties as a consequence of focal photothrombotic brain lesions in rats. After i.v. application, Gf led to bright contrast in the lesions, but also the entire ipsilateral cortex on T1-weighted MRI. In contrast, enhancement after application of gadolinium diethylenetriamine-pentaacetic acid (Gd-DTPA), a common clinical indicator of BBB leakage was restricted to the lesions. Remote Gf enhancement was restricted in time to the first 24 h after photothrombosis and corresponded to a transient breakdown of the BBB as revealed by extravasation of the dye Evans blue. In conclusion, our study shows that Gf can visualize subtle disturbances of the BBB in three dimensions not detectable by Gd-DTPA. Upon entry into the central nervous system Gf most likely is locally trapped by interactions with extracellular matrix proteins. The unique properties of Gf hold promise as a more sensitive contrast agent for monitoring BBB disturbances in neurologic disorders, which appear more widespread than anticipated previously.

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Interleukin-1β-Induced Changes in Blood–Brain Barrier Permeability, Apparent Diffusion Coefficient, and Cerebral Blood Volume in the Rat Brain: A Magnetic Resonance Study

Cited by 208 publications

References 56 publications

Systemic Inflammatory Response Reactivates Immune-Mediated Lesions in Rat Brain

Systemic Inflammatory Response Reactivates Immune-Mediated Lesions in Rat Brain

Truncation of monocyte chemoattractant protein 1 by plasmin promotes blood–brain barrier disruption

Transient Widespread Blood—Brain Barrier Alterations after Cerebral Photothrombosis as Revealed by Gadofluorine M-Enhanced Magnetic Resonance Imaging

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