Clinical implications of leukocyte infiltration at the choroid plexus in (neuro)inflammatory disorders

Demeestere, Delphine; Libert, Claude; Vandenbroucke, Roosmarijn E.

doi:10.1016/j.drudis.2015.05.003

Cited by 54 publications

(43 citation statements)

References 136 publications

(300 reference statements)

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“…This was blocked by fingolimod (FTY720; a sphingosine-1-phosphate receptor modulator) treatment which also markedly reduced the brain injury in lipopolysaccharide-enhanced hypoxia/ischemia injury. In other neurological conditions, such as multiple sclerosis, traumatic brain injury, spinal cord injury and meningitis, as well as peripheral inflammation, there has been interest in the role of the CP in leukocyte entry into CSF and brain [3, 136, 137]. For example, Szmydynger-Chodobska et al [138, 139] found that the CP is a site of neutrophil and monocyte entry into the brain after traumatic brain injury (controlled cortical impact).…”

Section: Choroid Plexus As a Responder To Injurymentioning

confidence: 99%

The choroid plexus as a site of damage in hemorrhagic and ischemic stroke and its role in responding to injury

Xiang

Routhe

Wilkinson

et al. 2017

Fluids Barriers CNS

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While the impact of hemorrhagic and ischemic strokes on the blood–brain barrier has been extensively studied, the impact of these types of stroke on the choroid plexus, site of the blood-CSF barrier, has received much less attention. The purpose of this review is to examine evidence of choroid plexus injury in clinical and preclinical studies of intraventricular hemorrhage, subarachnoid hemorrhage, intracerebral hemorrhage and ischemic stroke. It then discusses evidence that the choroid plexuses are important in the response to brain injury, with potential roles in limiting damage. The overall aim of the review is to highlight deficiencies in our knowledge on the impact of hemorrhagic and ischemic strokes on the choroid plexus, particularly with reference to intraventricular hemorrhage, and to suggest that a greater understanding of the response of the choroid plexus to stroke may open new avenues for brain protection.

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Section: Choroid Plexus As a Responder To Injurymentioning

confidence: 99%

The choroid plexus as a site of damage in hemorrhagic and ischemic stroke and its role in responding to injury

Xiang

Routhe

Wilkinson

et al. 2017

Fluids Barriers CNS

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“…Accordingly, the choroid plexus system is actively involved in physiological processes and is essential for maintaining brain homeostasis (Vandenbroucke, ). The choroid plexus is also an important sensor of inflammatory stimuli in the blood (Vandenbroucke et al , ; Balusu et al , ,b), and it may act as a selective gateway to the brain for the trafficking of immune cells (Demeestere et al , ). However, in AD this gateway system is altered, resulting in suboptimal recruitment of inflammation‐resolving immune cells to the brain (Baruch et al , ).…”

Section: Introductionmentioning

confidence: 99%

Counteracting the effects of TNF receptor‐1 has therapeutic potential in Alzheimer's disease

et al. 2018

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Alzheimer's disease (AD) is the most common form of dementia, and neuroinflammation is an important hallmark of the pathogenesis. Tumor necrosis factor (TNF) might be detrimental in AD, though the results coming from clinical trials on anti‐TNF inhibitors are inconclusive. TNFR1, one of the TNF signaling receptors, contributes to the pathogenesis of AD by mediating neuronal cell death. The blood–cerebrospinal fluid (CSF) barrier consists of a monolayer of choroid plexus epithelial (CPE) cells, and AD is associated with changes in CPE cell morphology. Here, we report that TNF is the main inflammatory upstream mediator in choroid plexus tissue in AD patients. This was confirmed in two murine AD models: transgenic APP/PS1 mice and intracerebroventricular (icv) AβO injection. TNFR1 contributes to the morphological damage of CPE cells in AD, and TNFR1 abrogation reduces brain inflammation and prevents blood–CSF barrier impairment. In APP/PS1 transgenic mice, TNFR1 deficiency ameliorated amyloidosis. Ultimately, genetic and pharmacological blockage of TNFR1 rescued from the induced cognitive impairments. Our data indicate that TNFR1 is a promising therapeutic target for AD treatment.

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“…To prevent disturbance of brain homeostasis due to alterations in the systemic blood composition, the brain is protected by a series of barriers, including the blood-brain barrier (BBB) and the blood-cerebrospinal fluid (CSF) barrier (De Bock et al, 2014). It has been suggested that systemic inflammation may contribute to the impairment of the BBB (Kortekaas et al, 2005;Stolp and Dziegielewska, 2009) and the blood-CSF barrier (Demeestere et al, 2015;Marques et al, 2009Marques et al, , 2007Vandenbroucke et al, 2012). Furthermore, multiple neurodegenerative disorders, including Parkinson's disease and Alzheimer's disease, have been associated with disruption of the BBB (Lee and Pienaar, 2014;Li et al, 2015;Stolp and Dziegielewska, 2009) and the blood-CSF barrier (Balusu et al, 2016a;Bergen et al, 2015;Brkic et al, 2015;Gorle et al, 2016;Pisani et al, 2012;Vandenbroucke, 2016;Vawter et al, 1996).…”

Section: Introductionmentioning

confidence: 99%

The choroid plexus epithelium as a novel player in the stomach-brain axis during Helicobacter infection

Gorlé

Blaecher

Bauwens

et al. 2018

Brain, Behavior, and Immunity

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Several studies suggest a link between shifts in gut microbiota and neurological disorders. Recently, we reported a high prevalence of Helicobacter suis (H. suis) in patients with Parkinson's disease. Here, we evaluated the effect of gastric H. suis infection on the brain in mice. One month of infection with H. suis resulted in increased brain inflammation, reflected in activation of microglia and cognitive decline. Additionally, we detected choroid plexus inflammation and disruption of the epithelial blood-cerebrospinal fluid (CSF) barrier upon H. suis infection, while the endothelial blood-brain barrier (BBB) remained functional. These changes were accompanied by leakage of the gastrointestinal barrier and low-grade systemic inflammation, suggesting that H. suis-evoked gastrointestinal permeability and subsequent peripheral inflammation induces changes in brain homeostasis via changes in blood-CSF barrier integrity. In conclusion, this study shows for the first time that H. suis infection induces inflammation in the brain associated with cognitive decline and that the choroid plexus is a novel player in the stomach-brain axis.

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Clinical implications of leukocyte infiltration at the choroid plexus in (neuro)inflammatory disorders

Cited by 54 publications

References 136 publications

The choroid plexus as a site of damage in hemorrhagic and ischemic stroke and its role in responding to injury

The choroid plexus as a site of damage in hemorrhagic and ischemic stroke and its role in responding to injury

Counteracting the effects of TNF receptor‐1 has therapeutic potential in Alzheimer's disease

The choroid plexus epithelium as a novel player in the stomach-brain axis during Helicobacter infection

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