Human serum amyloid P component attenuates the bacterial lipopolysaccharide-induced increase in blood–brain barrier permeability in mice

Veszelka, Szilvia

doi:10.1016/s0304-3940(03)01013-9

Cited by 11 publications

(14 citation statements)

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“…SAP treatment alone did not change brain endothelial paracellular permeability or morphology. In a previous in vivo study, when mice were injected with human SAP no deleterious effect on paracellular permeability was noticed [60]. Based on these observations, SAP in physiological concentrations has no effect on brain endothelial TJs.…”

Section: Studies With Aβ On Culture-based Bbb Modelsmentioning

confidence: 69%

Protection of the Blood-Brain Barrier by Pentosan Against Amyloid-β-Induced Toxicity

Deli

Veszelka

Csiszár

et al. 2010

JAD

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Abstract. Endothelial cells of brain capillaries forming the blood-brain barrier play an important role in the pathogenesis and therapy of Alzheimer's disease. Amyloid-β (Aβ) peptides are key pathological elements in the development of the disease. A blood-brain barrier model, based on primary rat brain endothelial cells was used in which the barrier properties were induced by glial cells. The effects of amyloid peptides have been tested on cell viability and barrier functions. Aβ showed toxic effects on primary rat brain endothelial cells measured by MTT dye conversion and the lactate dehydrogenase release. Morphologically cytoplasmic vacuolization, disruption of the structure of cytoplasmic organelles and tight junctions could be observed in brain endothelial cells. Treatment with Aβ1−42 decreased the electrical resistance, and increased the permeability of brain endothelial cell monolayers for both fluorescein and albumin. Serum amyloid P component which stabilizes Aβ fibrils in cortical amyloid plaques and cerebrovascular amyloid deposits significantly potentiated the barrier-weakening effect of Aβ1−42. Sulfated polysaccharide pentosan could decrease the toxic effects of Aβ peptides in brain endothelial cells. It could also significantly protect the barrier integrity of monolayers from damaging actions of peptides. Pentosan modified the size, and significantly decreased the number of amyloid aggregates demonstrated by atomic force microscopy. The present data further support the toxic effects of amyloid peptides on brain endothelial cells, and can contribute to the development of molecules protecting the blood-brain barrier in Alzheimer's disease.

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Section: Studies With Aβ On Culture-based Bbb Modelsmentioning

confidence: 69%

Protection of the Blood-Brain Barrier by Pentosan Against Amyloid-β-Induced Toxicity

Deli

Veszelka

Csiszár

et al. 2010

JAD

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“…Treatment of mice with a low dose of LPS (3 mg/kg) partially compromises the integrity of the BBB without disrupting the capillary structure (9,69), and this approach has been used to investigate the in vivo capacity of factors to modulate BBB permeability (1,63). We postulated that LPS-mediated compromise of the BBB is relevant to HIV-1 infection because the BBB in HIV-1-infected individuals may be partially compromised in a similar manner by their increased levels of LPS in plasma (11).…”

Section: Resultsmentioning

confidence: 99%

Human Immunodeficiency Virus Type 1 Infection Increases the In Vivo Capacity of Peripheral Monocytes To Cross the Blood-Brain Barrier into the Brain and the In Vivo Sensitivity of the Blood-Brain Barrier to Disruption by Lipopolysaccharide

Wang¹,

Sun²,

Goldstein

2008

J Virol

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Human immunodeficiency virus type 1 (HIV-1), introduced into the brain by HIV-1-infected monocytes which migrate across the blood-brain barrier (BBB), infects resident macrophages and microglia and initiates a process that causes HIV-1-associated neurocognitive disorders. The mechanism by which HIV-1 infection circumvents the BBB-restricted passage of systemic leukocytes into the brain and disrupts the integrity of the BBB is not known. Circulating lipopolysaccharide (LPS), which can compromise the integrity of the BBB, is significantly increased in HIV-1-infected individuals. We hypothesized that HIV-1 infection increases monocyte capacity to migrate across the BBB, which is further facilitated by a compromise of BBB integrity mediated by the increased systemic LPS levels present in HIV-1-infected individuals. To investigate this possibility, we examined the in vivo BBB migration of monocytes derived from our novel mouse model, JR-CSF/EYFP mice, which are transgenic for both a long terminal repeat-regulated full-length infectious HIV-1 provirus and ROSA-26-regulated enhanced yellow fluorescent protein. We demonstrated that JR-CSF/EYFP mouse monocytes displayed an increased capacity to enter the brain by crossing either an intact BBB or a BBB whose integrity was partially compromised by systemic LPS. We also demonstrated that the JR-CSF mouse BBB was more susceptible to disruption by systemic LPS than the control wild-type mouse BBB. These results demonstrated that HIV-1 infection increased the ability of monocytes to enter the brain and increased the sensitivity of the BBB to disruption by systemic LPS, which is elevated in HIV-1-infected individuals. These mice represent a new in vivo system for studying the mechanism by which HIV-1-infected monocytes migrate into the brain.

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“…Rather, larger molecular weight reagents such as Evans blue, radioactive albumin and fluorescent-IgG have been used (Tachibana et al 1981;Kastenbauer et al 2001;Trune 1997). Others have measured the dye content of tissue homogenates, but this application in assessment of inner ear vascular permeability has been met with limited success (Rossner and Tempel 1966;Veszelka et al 2003;Awad 2006). When used in the inner ear, these techniques demonstrate shortcomings due to high levels of contamination from dyes that leach out of the cochlear vessels during tissue processing.…”

Section: Figmentioning

confidence: 99%

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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Human serum amyloid P component attenuates the bacterial lipopolysaccharide-induced increase in blood–brain barrier permeability in mice

Cited by 11 publications

References 0 publications

Protection of the Blood-Brain Barrier by Pentosan Against Amyloid-β-Induced Toxicity

Protection of the Blood-Brain Barrier by Pentosan Against Amyloid-β-Induced Toxicity

Human Immunodeficiency Virus Type 1 Infection Increases the In Vivo Capacity of Peripheral Monocytes To Cross the Blood-Brain Barrier into the Brain and the In Vivo Sensitivity of the Blood-Brain Barrier to Disruption by Lipopolysaccharide

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

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