Permeability of the blood–cerebrospinal fluid barrier to plasma proteins during foetal and perinatal life

Adinolfí, Matteo; Beck, Susan E.; Haddad, Susan A.; Seller, Mary J.

doi:10.1038/259140a0

Cited by 93 publications

(29 citation statements)

References 16 publications

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“…before the challenge, but none of the rats were protected against infection. Adinolfi et al [1] inoculated i.p. labeled IgG antibody into 1-day-old rats and found that, after 3 hr, the level of the IgG in the cerebrospinal fluid was about 10% of that in blood.…”

Section: Discussionmentioning

confidence: 98%

Characteristics of passive immunity against hantavirus infection in rats

Zhang

Takashima

Hashimoto

1989

Archives of Virology

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The protective effects of passively administered antibodies against hantavirus infection were studied in newborn rats. Death as well as infection were completely prevented from intraperitoneal challenge of strain SR-11 (SR) (2 x 10(3) FFU, 10(2.1) LD50), in newborn rats which received 0.1 ml of anti-SR rat serum (neutralizing antibody titer, 1:640) 4 hr before the virus challenge. In these rats, no virus was detected in the peritoneal macrophages, lung, kidney, and brain. The immune serum infusion before the virus challenge also conferred protection to rats against an intramuscular or subcutaneous challenge of strain SR, but did not protect the rats against intracerebral challenge of the virus. In the rats which received the immune serum after the challenge, infection was not prevented, although some of the animals were protected from the death. Virus titers in the lung, kidney, and brain of the rats were reduced by the transfer of the immune serum even as late as 72 hr after the challenge. Cross-protection in the rats which received the immune serum was strong between strains SR and KI-262 within the same serotype, but very weak between strains SR and Hantaan 76-118 of different serotypes.

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Section: Discussionmentioning

confidence: 98%

Characteristics of passive immunity against hantavirus infection in rats

Zhang

Takashima

Hashimoto

1989

Archives of Virology

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“…The morphological basis of these barriers is dependent on intercellular junctions that occlude paracellular transfer of lipid insoluble molecules from the very earliest stages of brain development [1], [2]. In spite of this physical barrier the concentration of protein in fetal CSF is well known to be much higher than in the adult in all animal species studied [3]–[12]. In addition it has been shown previously that the proteins present in the CSF are mostly derived from blood plasma [10], [11], [13]–[15] and enter the ventricular system by a developmentally regulated transfer across a population of specialised choroid plexus epithelial cells [16].…”

Section: Introductionmentioning

confidence: 99%

Cellular Specificity of the Blood–CSF Barrier for Albumin Transfer across the Choroid Plexus Epithelium

et al. 2014

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To maintain the precise internal milieu of the mammalian central nervous system, well-controlled transfer of molecules from periphery into brain is required. Recently the soluble and cell-surface albumin-binding glycoprotein SPARC (secreted protein acidic and rich in cysteine) has been implicated in albumin transport into developing brain, however the exact mechanism remains unknown. We postulate that SPARC is a docking site for albumin, mediating its uptake and transfer by choroid plexus epithelial cells from blood into cerebrospinal fluid (CSF). We used in vivo physiological measurements of transfer of endogenous (mouse) and exogenous (human) albumins, in situ Proximity Ligation Assay (in situ PLA), and qRT-PCR experiments to examine the cellular mechanism mediating protein transfer across the blood–CSF interface. We report that at all developmental stages mouse albumin and SPARC gave positive signals with in situ PLAs in plasma, CSF and within individual plexus cells suggesting a possible molecular interaction. In contrast, in situ PLA experiments in brain sections from mice injected with human albumin showed positive signals for human albumin in the vascular compartment that were only rarely identifiable within choroid plexus cells and only at older ages. Concentrations of both endogenous mouse albumin and exogenous (intraperitoneally injected) human albumin were estimated in plasma and CSF and expressed as CSF/plasma concentration ratios. Human albumin was not transferred through the mouse blood–CSF barrier to the same extent as endogenous mouse albumin, confirming results from in situ PLA. During postnatal development Sparc gene expression was higher in early postnatal ages than in the adult and changed in response to altered levels of albumin in blood plasma in a differential and developmentally regulated manner. Here we propose a possible cellular route and mechanism by which albumin is transferred from blood into CSF across a sub-population of specialised choroid plexus epithelial cells.

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“…Experiments performed in the late 1950’s demonstrated when female mice were immunized with a brain emulsion and later mated, subsequent offspring had gross brain abnormalities, which the author attributed to maternal antibodies directed against the brain and nervous system of the embryos(42). This idea gained favor again in the early 1970’s, when researchers, concerned that maternal environmental exposures could have detrimental effects on fetal nervous system development, discovered maternal IgG was present in fetal cerebral spinal fluid (CSF), and was able to gain access to brain during gestation and early life due the permissive nature of the blood brain barrier during that period(43–45). Succeeding experiments by several groups showed that antibrain antibodies could induce behavioral changes in the exposed offspring(46, 47).…”

Section: The Detection Of Autoantibodies In Asdmentioning

confidence: 99%

Autoimmunity, Autoantibodies, and Autism Spectrum Disorder

Edmiston

Ashwood

Water

2017

Biological Psychiatry

119

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Autism spectrum disorder (ASD) now affects one in 68 births in the United States and is the fastest growing neurodevelopmental disability worldwide. Alarmingly, for the majority of cases, the causes of ASD are largely unknown, but it is becoming increasingly accepted that ASD is no longer defined simply as a behavioral disorder, but rather as a highly complex and heterogeneous biological disorder. While research has focused on the identification of genetic abnormalities, emerging studies increasingly suggest immune dysfunction is a viable risk factor contributing to the neurodevelopmental deficits observed in ASD. This review summarizes the investigations implicating autoimmunity and autoantibodies in ASD.

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Permeability of the blood–cerebrospinal fluid barrier to plasma proteins during foetal and perinatal life

Cited by 93 publications

References 16 publications

Characteristics of passive immunity against hantavirus infection in rats

Characteristics of passive immunity against hantavirus infection in rats

Cellular Specificity of the Blood–CSF Barrier for Albumin Transfer across the Choroid Plexus Epithelium

Autoimmunity, Autoantibodies, and Autism Spectrum Disorder

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