Spatiotemporal induction patterns of cytokine and related immune signal molecule mRNAs in response to intrastriatal injection of lipopolysaccharide

Stern, Edra L; Quan, Ning; Proescholdt, Margit G.; Herkenham, Miles

doi:10.1016/s0165-5728(00)00318-0

Cited by 35 publications

(6 citation statements)

References 85 publications

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“…On the other hand, high circulating levels of the endotoxin are associated with an increased expression of a number of inflammatory genes across the brain parenchyma (8,(11)(12)(13). Such widespread induction that was not observed in response to an IS LPS infusion is in agreement with another recent study (14). This rather localized hybridization signal ipsilateral to the site of infusion may also be dependent on the dose of LPS, which was not verified in the present study.…”

Section: Discussionsupporting

confidence: 81%

Endotoxemia Prevents the Cerebral Inflammatory Wave Induced by Intraparenchymal Lipopolysaccharide Injection: Role of Glucocorticoids and CD14

Nadeau

Rivest

2002

The Journal of Immunology

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There is a robust and transient innate immune response in the brain during endotoxemia, which is associated with a cascade of NF-κB signaling events and transcriptional activation of genes that encode TNF-α and the LPS receptor CD14. The present study investigated whether circulating LPS has the ability to modulate the cerebral innate immune response caused by an intrastriatal (IS) injection of the endotoxin. We also tested the possibility that CD14 plays a role in these effects and male rats received an intracerebroventricular injection with an anti-CD14 before the IS LPS administration. The single LPS bolus into the striatum caused a strong and time-dependent transcriptional activation of TNF-α, IκBα, CD14, and monocyte chemoattractant protein-1 mRNA in microglial cells ipsilateral to the site of injection. Surprisingly, this wave of induced transcripts was essentially abolished by the systemic endotoxin pretreatment. Such anti-inflammatory properties of circulating LPS are mediated via plasma corticosterone, because exogenous corticoids mimicked while glucocorticoid receptor antagonist RU486 prevented the effects of systemic endotoxin challenge. Of interest is the partial involvement of CD14 in LPS-induced neuroinflammation; the anti-CD14 significantly abolished the microglial activity at day 3, but not at times earlier. The inflammatory response provoked by an acute intraparenchymal LPS bolus was not associated with convincing neurodegenerative processes. These data provide compelling evidence that systemic inflammation, through the increase in circulating glucocorticoids, has the ability to prevent the cerebral innate immune reaction triggered by an IS endotoxin injection. This study also further consolidates the existence of such system in the brain, which is finely regulated and its transient activation is not harmful for the neuronal elements.

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Section: Discussionsupporting

confidence: 81%

Endotoxemia Prevents the Cerebral Inflammatory Wave Induced by Intraparenchymal Lipopolysaccharide Injection: Role of Glucocorticoids and CD14

Nadeau

Rivest

2002

The Journal of Immunology

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“…4). This postlesion time is associated with maximal cytokine production, a microglia activation marker (Stern et al, 2000), that precedes the death of nigral DA neuons. Benzamide treatment failed to alter LPS-induced microglia activation (Fig.…”

Section: In Vivo Inhibition Of Aif Signaling But Not Of Caspase-3 Cmentioning

confidence: 99%

Apoptosis-inducing factor mediates dopaminergic cell death in response to LPS-induced inflammatory stimulus

Burguillos¹,

Hajji²,

Englund³

et al. 2011

Neurobiology of Disease

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We show that intranigral lipopolysaccharide (LPS) injection, which provokes specific degeneration of DA neurons, induced caspase-3 activation in the rat ventral mesencephalon, which was mostly associated with glial cells. In contrast, nigral DA neurons exhibited AIF nuclear translocation in response to LPS. A significant decrease of the Bcl-2/Bax ratio in nigral tissue after LPS injection was observed. We next developed an in vitro co-culture system with the microglial BV2 and the DA neuronal MN9D murine cell lines. The

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“…A single cancer cell, for example, can kill an organism by forming a tumour, 1 localised enzyme production can create gradients of diffusive retinoic acid that patterns a growing organism, 2 the global heart pumping rate is controlled by a few local pacemaker cells, 3 single bacteria can sense each other in close proximity and build a colony by quorum sensing 4 and localized invading bacteria and viruses activate a global inflammatory response. 5 Common to these examples is a spatially and temporally localized environmental input acting on a small group of cells, from where information spreads via cell-cell interactions to tissue by activating genetically encoded signalling pathways.…”

Section: Introductionmentioning

confidence: 99%

Automated co-culture system for spatiotemporal analysis of cell-to-cell communication

Frank

Tay

2015

Lab Chip

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We present a microfluidic co-culture system that generates localized and precisely formulated immune signals among a population of cells, enabling spatiotemporal analysis of paracrine signal transmission between different cell types. The automated system allows us to create temporally modulated chemical inputs that can be delivered to single signal-transmitting and receiving cells in a highly controlled way. Using this system we stimulated a single macrophage with brief pulses of bacterial LPS and observed the macrophage transmitted TNF signal propagating in a population of fibroblasts via NF-κB activation. The signal receiving fibroblasts transformed the TNF signal into a spatiotemporally distributed NF-κB output, recapitulating the initiation of immune response to bacterial infection.

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Spatiotemporal induction patterns of cytokine and related immune signal molecule mRNAs in response to intrastriatal injection of lipopolysaccharide

Cited by 35 publications

References 85 publications

Endotoxemia Prevents the Cerebral Inflammatory Wave Induced by Intraparenchymal Lipopolysaccharide Injection: Role of Glucocorticoids and CD14

Endotoxemia Prevents the Cerebral Inflammatory Wave Induced by Intraparenchymal Lipopolysaccharide Injection: Role of Glucocorticoids and CD14

Apoptosis-inducing factor mediates dopaminergic cell death in response to LPS-induced inflammatory stimulus

Automated co-culture system for spatiotemporal analysis of cell-to-cell communication

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