Haemophilus influenzae lipopolysaccharide-induced blood brain barrier permeability during experimental meningitis in the rat.

Wispelwey, Brian; Lesse, Alan J.; Hansen, Eric J.; Scheld, W. Michael

doi:10.1172/jci113736

Cited by 196 publications

(117 citation statements)

References 41 publications

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“…These findings are consistent with other studies that demonstrate compromise of the blood-brain barrier in LPS-pretreated animals (Jangula and Murphy 2013; Wispelwey et al 1988;Cardona et al 2008). A compromised blood-brain barrier has also been found in animals with experimental models of multiple sclerosis and in infectious conditions of the brain and spinal cord (Nadeau and Rivest 2002;Wispelwey et al 1988;Charlier et al 2009;Lustig et al 1992;McCandless et al 2008;Diamond and Klein 2004). The difference between fluorescein content in the perilymph versus that in the CSF may be reflecting the fact that there is a higher volume of CSF than perilymph and therefore a more diluted pool of fluorescein, and that there are a greater density of vessels in contact with perilymph than there are vessels in contact with CSF.…”

Section: Differences In Fluorescein Content Comparing Perilymph To Cssupporting

confidence: 93%

“…As expected, the fluorescein percentage present in the CSF was also higher in LPS pretreated mice than in control mice. These findings are consistent with other studies that demonstrate compromise of the blood-brain barrier in LPS-pretreated animals (Jangula and Murphy 2013; Wispelwey et al 1988;Cardona et al 2008). A compromised blood-brain barrier has also been found in animals with experimental models of multiple sclerosis and in infectious conditions of the brain and spinal cord (Nadeau and Rivest 2002;Wispelwey et al 1988;Charlier et al 2009;Lustig et al 1992;McCandless et al 2008;Diamond and Klein 2004).…”

Section: Differences In Fluorescein Content Comparing Perilymph To Cssupporting

confidence: 92%

“…Traditional studies in the central nervous system have employed methods such as dye exclusion tests, radioactive tracers, as well as in vitro models to assess the integrity of the BLB and the BBB (Rossner and Tempel 1966;Wispelwey et al 1988;Zhang et al 2013). Agents such as Evans blue dye or fluoresceintagged molecules can be effective to determine sites of vascular leakage where there are large volumes of tissue that are sparsely vascularized (Nishioku et al 2009;Fernandez-Lopez et al 2012;He et al 2014).…”

Section: Introductionmentioning

confidence: 99%

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Systemic Lipopolysaccharide Compromises the Blood-Labyrinth Barrier and Increases Entry of Serum Fluorescein into the Perilymph

Hirose

Hartsock

Johnson

et al. 2014

JARO

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The blood vessels that supply the inner ear form a barrier between the blood and the inner ear fluids to control the exchange of solutes, protein, and water. This barrier, called the blood-labyrinth barrier (BLB) is analogous to the blood-brain barrier (BBB), which plays a critical role in limiting the entry of inflammatory and infectious agents into the central nervous system. We have developed an in vivo method to assess the functional integrity of the BLB by injecting sodium fluorescein into the systemic circulation of mice and measuring the amount of fluorescein that enters perilymph in live animals. In these experiments, perilymph was collected from control and experimental mice in sequential samples taken from the posterior semicircular canal approximately 30 min after systemic fluorescein administration. Perilymph fluorescein concentrations in control mice were compared with perilymph fluorescein concentrations after lipopolysaccharide (LPS) treatment (1 mg/kg IP daily for 2 days). The concentration of perilymphatic fluorescein, normalized to serum fluorescein, was significantly higher in LPS-treated mice compared to controls. In order to assess the contributions of perilymph and endolymph in our inner ear fluid samples, sodium ion concentration of the inner ear fluid was measured using ion-selective electrodes. The sampled fluid from the posterior semicircular canal demonstrated an average sodium concentration of 145 mM, consistent with perilymph. These experiments establish a novel technique to assess the functional integrity of the BLB using quantitative methods and to provide a comparison of the BLB to the BBB.

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Section: Differences In Fluorescein Content Comparing Perilymph To Cssupporting

confidence: 93%

Section: Differences In Fluorescein Content Comparing Perilymph To Cssupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Systemic Lipopolysaccharide Compromises the Blood-Labyrinth Barrier and Increases Entry of Serum Fluorescein into the Perilymph

Hirose

Hartsock

Johnson

et al. 2014

JARO

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“…71 Also, elevated levels of lipopolysaccharide as a result of bacterial infection can compromise the BBB. 72,73 Lipopolysaccharide can also increase endocytic activity of brain microendothelial cells. 74 It is possible that JCPyV already bound to the neuroendothelium enters the brain parenchyma after transient disruption of the BBB.…”

Section: Direct Binding Of Jcpyv To Barriers Of the Cnsmentioning

confidence: 99%

Human Polyomavirus Receptor Distribution in Brain Parenchyma Contrasts with Receptor Distribution in Kidney and Choroid Plexus

Haley

O’Hara

Nelson

et al. 2015

The American Journal of Pathology

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The human polyomavirus, JCPyV, is the causative agent of progressive multifocal leukoencephalopathy, a rare demyelinating disease that occurs in the setting of prolonged immunosuppression. After initial asymptomatic infection, the virus establishes lifelong persistence in the kidney and possibly other extraneural sites. In rare instances, the virus traffics to the central nervous system, where oligodendrocytes, astrocytes, and glial precursors are susceptible to lytic infection, resulting in progressive multifocal leukoencephalopathy. The mechanisms by which the virus traffics to the central nervous system from peripheral sites remain unknown. Lactoseries tetrasaccharide c (LSTc), a pentasaccharide containing a terminal a2,6elinked sialic acid, is the major attachment receptor for polyomavirus. In addition to LSTc, type 2 serotonin receptors are required for facilitating virus entry into susceptible cells. We studied the distribution of virus receptors in kidney and brain using lectins, antibodies, and labeled virus. The distribution of LSTc, serotonin receptors, and virus binding sites overlapped in kidney and in the choroid plexus. In brain parenchyma, serotonin receptors were expressed on oligodendrocytes and astrocytes, but these cells were negative for LSTc and did not bind virus. LSTc was instead found on microglia and vascular endothelium, to which virus bound abundantly. Receptor distribution was not changed in the brains of patients with progressive multifocal leukoencephalopathy. Virus infection of oligodendrocytes and astrocytes during disease progression is LSTc independent. (Am J Pathol 2015, 185: 2246e2258; http://dx.doi.org/10.1016/j.ajpath.2015.04.003)The human polyomavirus (JCPyV) is the causative agent of progressive multifocal leukoencephalopathy (PML), a rapidly progressing, often fatal neurodegenerative disease. Although PML is rare, JCPyV infection is widespread, infecting approximately 50% to 80% of the healthy adult population. 1,2 As the initial infection is asymptomatic, the mode of JCPyV transmission is unknown. The virus establishes a persistent infection in the kidney and urinary tract of immunocompetent hosts, 3 and about 20% of these infected individuals shed virus in their urine. 4 JCPyV DNA has also been detected in other tissues, including B lymphocytes in the bone marrow, tonsillar stromal cells, lungs, spleen, and brain, 5e13 suggesting additional sites of viral persistence. The route of viral transmission from the initial site(s) of infection and latency to the central nervous system (CNS), the main site of pathogenesis, is not clearly understood.Under conditions of immunosuppression, JCPyV infects and destroys the myelin-producing oligodendrocytes, resulting in demyelination, which is the hallmark of this fatal disease; to a Supported by NIH grants R01NS043097 (W.J.A.) and P01NS065719 (W.J.A.).

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“…For instance, the time over which neutrophils infiltrate an ischemic stroke (beginning at 6h in experimental studies in the rat (Barone et al, 1995) and 15h in humans (Lindsberg et al, 1996) and persisting for days) mirrors edema development, suggesting that neutrophils could be causal factors (Lindsberg et al, 1996;Zhang et al, 1994, Del Zoppo et al, 2001). However studies in animal disease models have been contradictory, with some correlating neutrophils to indicators of brain edema (Del Maschio et al, 1999;Matsuo et al, 1994;Wispelwey et al, 1988;Yamasaki et al, 1995). Others show no relationship (Adelson et al, 1998;Hartl et al, 1997;Tauber et al, 1988;Whalen et al, 1999) while others suggest that neutrophils reduce BBB disruption (Ahmed et al, 2000;Lo et al, 1998;Schurer et al, 1990).…”

Section: Accepted M Manuscriptmentioning

confidence: 99%

Modulation of blood–brain barrier permeability by neutrophils: in vitro and in vivo studies

et al. 2009

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Abstract.The blood-brain barrier (BBB) restricts solute permeability across healthy cerebral endothelial cells. However, during inflammation, permeability is increased and can lead to deleterious cerebral edema. Neutrophils are early cellular participants in acute inflammation, but their effect on BBB permeability is unclear. To study this, neutrophils were applied in a resting and activated state to in vitro and in vivo models of the BBB. In vitro, human neutrophils (5 X 10 6 /ml) were activated with tumor necrosis factor (100U/ml) and leukotriene B 4 (10 -7 mol/l).Untreated neutrophils reduced permeability across the human brain endothelial cell line hCMEC/ D3. Activated neutrophils returned permeability to baseline, an effect blocked by the reactive oxygen scavengers superoxide dismutase (10U/ml) and catalase (1000U/ml). In vivo, human neutrophils (2.5 X 10 5 in 4μl) were injected into the striatum of anesthetized juvenile Wistar rats, and BBB permeability measured 30 minutes later. This was compared to control injections (4μl) of vehicle (0.9% saline) and arachidonic acid (10 -3 mol/l). The injection generated a small hematoma around the injection tract (<3μl). Untreated neutrophils induced significantly lower permeability in their vicinity than activated neutrophils, with a trend to lowered permeability compared to the vehicle control. Neither untreated nor activated neutrophils induced permeability increases, while arachidonic acid increased permeability as a positive control. This study further delineates the effect of neutrophils on the BBB, and demonstrates that resting neutrophils induce acute reductions in permeability while activated neutrophils have a neutral effect. The in vivo model reiterates some aspects of acute intracerebral hemorrhage.Section: Cellular and molecular biology of nervous systems.

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Haemophilus influenzae lipopolysaccharide-induced blood brain barrier permeability during experimental meningitis in the rat.

Cited by 196 publications

References 41 publications

Systemic Lipopolysaccharide Compromises the Blood-Labyrinth Barrier and Increases Entry of Serum Fluorescein into the Perilymph

Systemic Lipopolysaccharide Compromises the Blood-Labyrinth Barrier and Increases Entry of Serum Fluorescein into the Perilymph

Human Polyomavirus Receptor Distribution in Brain Parenchyma Contrasts with Receptor Distribution in Kidney and Choroid Plexus

Modulation of blood–brain barrier permeability by neutrophils: in vitro and in vivo studies

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