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The circumventricular organs participate in the immunopathogenesis of experimental autoimmune encephalomyelitis
Martina Schulz, Britta Engelhardt
Fluids and Barriers of the CNS , 2005, DOI: 10.1186/1743-8454-2-8
Abstract: We performed an extensive immunohistological study on the area postrema (AP), the subfornical organ (SFO), the organum vasculosum of the lamina terminalis (OVLT) and the median eminence (ME) in frozen brain sections from healthy SJL mice and mice suffering from EAE. Expression of cell adhesion molecules, the presence of leukocyte subpopulations and the detection of major histocompatibility complex antigen expression was compared.Similar changes were observed for all four CVOs included in this study. During EAE significantly increased numbers of CD45+ leukocytes were detected within the four CVOs investigated, the majority of which stained positive for the macrophage markers F4/80 and Mac-1. The adhesion molecules ICAM-1 and VCAM-1 were upregulated on the fenestrated capillaries within the CVOs. A considerable upregulation of MHC class I throughout the CVOs and positive immunostaining for MHC class II on perivascular cells additionally documented the immune activation of the CVOs during EAE. A significant enrichment of inflammatory infiltrates was observed in close vicinity to the CVOs.Our data indicate that the CVOs are a site for the entry of immune cells into the CNS and CSF and consequently are involved in the inflammatory process in the CNS during EAE.In multiple sclerosis and in its animal model, experimental autoimmune encephalomyelitis (EAE), inflammatory cells obtain access to the central nervous system (CNS) parenchyma and the cerebrospinal fluid (CSF) and initiate the events leading to signs of paralysis. The endothelial blood-brain barrier (BBB) has been considered the obvious place for entry for circulating lymphocytes into the CNS. Therefore most investigations have focused on defining the molecular mechanisms involved in leukocyte recruitment from the circulating blood across the endothelial BBB. The adhesion molecules, intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1), both members of the immunoglobulin superfam
Circumventricular organs of rats that experimental hydrocephalus and subarachnoidal hemorrhage carried out: an anaglyphic SEM study  [PDF]
Tatar I,Akpinar G,Acikgoz B,Tunali S
Neuroanatomy , 2004,
Abstract: It is known that circumventricular organs that are located around the ventricular system ofthe brain are lack of blood-brain barrier and support the body water-salt balance. They alsoeffect many physiological events such as some neuroendocrine and reproduction mechanisms.In different pathological conditions their results and the step in which the circumventricularorgans are affected are unknown. Although circumventricular organs do not have a bloodbrainbarrier, they do not completely show the same characteristics.In pathological conditions they show their own effects by means of mediators. It is necessaryto research their structural changes, also the changes in the neurotransmitters that areaffected by circumventricular organs.Hydrocephalus was induced in rats by injecting kaolin into the subarachnoidal space at thecranial convexity. Subarachnoidal hemorrhage was realized with a puncture of the basilarartery through transclival route. We took and studied images using a JEOL SEM ASID-10(Japan) electron microscope. We examined slices of subfornical organ, organum vasculosum,lamina terminalis, area postrema and median eminence.The purpose of this study is to view three-dimensional scanning electron microscopicimages of the circumventricular organs using the anaglyph technique that records images asstereopairs (converted as a red-blue images and viewed with special glasses).
Interleukin-10 modulates the synthesis of inflammatory mediators in the sensory circumventricular organs: implications for the regulation of fever and sickness behaviors  [cached]
Harden Lois M,Rummel Christoph,Luheshi Giamal N,Poole Stephen
Journal of Neuroinflammation , 2013, DOI: 10.1186/1742-2094-10-22
Abstract: Background Whereas the role played by interleukin (IL)-10 in modulating fever and sickness behavior has been linked to it targeting the production of pro-inflammatory cytokines in the circulation, liver and spleen, it is not known whether it could directly target the local production of pro-inflammatory cytokines within the sensory circumventricular organs (CVOs) situated within the brain, but outside the blood–brain barrier. Using inactivation of IL-10, we, therefore, investigated whether IL-10 could modulate the synthesis of pro-inflammatory cytokines within the sensory CVOs, in particular the organum vasculosum laminae terminalis (OVLT) and area postrema (AP). Findings Primary OVLT and AP microcultures were established from topographically excised rat pup brain tissue. The microcultures were pretreated with either IL-10 antibodies (AB) (10 μl/350 μl medium) or phosphate-buffered saline (PBS) (10 μl/350 μl medium) before being incubated with lipopolysaccharide (LPS) (100 μg/ml) or PBS in complete medium for 6 h. Supernatants were removed from the microcultures after 6 h of incubation with LPS and used for the determination of IL-6 and tumor necrosis factor (TNF)-α. Pre-treating the OVLT and AP microcultures with IL-10 antibodies significantly enhanced the LPS-induced increase in TNF-α and IL-6 in the supernatant obtained from the microcultures. Conclusions Our results show for the first time that the LPS-induced release of pro-inflammatory cytokines in cells cultured from the AP and OVLT can be modulated in the presence of IL-10 antibodies. Thus, we have identified that the sensory CVOs may have a key role to play in both the initiation and modulation of neuroinflammation.
Gadofluorine M-enhanced MRI shows involvement of circumventricular organs in neuroinflammation
Eva Wuerfel, Carmen Infante-Duarte, Robert Glumm, Jens T Wuerfel
Journal of Neuroinflammation , 2010, DOI: 10.1186/1742-2094-7-70
Abstract: In a longitudinal study we investigated in vivo alterations of CVO during neuroinflammation, applying Gadofluorine M- (Gf) enhanced magnetic resonance imaging (MRI) in experimental autoimmune encephalomyelitis, an animal model of multiple sclerosis. SJL/J mice were monitored by Gadopentate dimeglumine- (Gd-DTPA) and Gf-enhanced MRI after adoptive transfer of proteolipid-protein-specific T cells. Mean Gf intensity ratios were calculated individually for different CVO and correlated to the clinical disease course. Subsequently, the tissue distribution of fluorescence-labeled Gf as well as the extent of cellular inflammation was assessed in corresponding histological slices.We could show that the Gf signal intensity of the choroid plexus, the subfornicular organ and the area postrema increased significantly during experimental autoimmune encephalomyelitis, correlating with (1) disease severity and (2) the delay of disease onset after immunization. For the choroid plexus, the extent of Gf enhancement served as a diagnostic criterion to distinguish between diseased and healthy control mice with a sensitivity of 89% and a specificity of 80%. Furthermore, Gf improved the detection of lesions, being particularly sensitive to optic neuritis. In correlated histological slices, Gf initially accumulated in the extracellular matrix surrounding inflammatory foci and was subsequently incorporated by macrophages/microglia.Gf-enhanced MRI provides a novel highly sensitive technique to study cerebral BBB alterations. We demonstrate for the first time in vivo the involvement of CVO during the development of neuroinflammation.The central nervous system (CNS) may no longer be considered immune privileged but rather a site of selective immune activity [1,2]. This so-called restricted immunity is warranted by the barrier function of capillary endothelium, which channels the entry of serum proteins and immune cells from the blood to the CNS or the cerebrospinal fluid (CSF), respectively [1
High Blood Pressure Effects on the Blood to Cerebrospinal Fluid Barrier and Cerebrospinal Fluid Protein Composition: A Two-Dimensional Electrophoresis Study in Spontaneously Hypertensive Rats  [PDF]
Ibrahim González-Marrero,Leandro Casta?eyra-Ruiz,Juan M. González-Toledo,Agustín Casta?eyra-Ruiz,Hector de Paz-Carmona,Rafael Castro,Juan R. Hernandez-Fernaud,Agustín Casta?eyra-Perdomo,Emilia M. Carmona-Calero
International Journal of Hypertension , 2013, DOI: 10.1155/2013/164653
Abstract: The aim of the present work is to analyze the cerebrospinal fluid proteomic profile, trying to find possible biomarkers of the effects of hypertension of the blood to CSF barrier disruption in the brain and their participation in the cholesterol and β-amyloid metabolism and inflammatory processes. Cerebrospinal fluid (CSF) is a system linked to the brain and its composition can be altered not only by encephalic disorder, but also by systemic diseases such as arterial hypertension, which produces alterations in the choroid plexus and cerebrospinal fluid protein composition. 2D gel electrophoresis in cerebrospinal fluid extracted from the cistern magna before sacrifice of hypertensive and control rats was performed. The results showed different proteomic profiles between SHR and WKY, that α-1-antitrypsin, apolipoprotein A1, albumin, immunoglobulin G, vitamin D binding protein, haptoglobin and α-1-macroglobulin were found to be up-regulated in SHR, and apolipoprotein E, transthyretin, α-2-HS-glycoprotein, transferrin, α-1β-glycoprotein, kininogen and carbonic anhidrase II were down-regulated in SHR. The conclusion made here is that hypertension in SHR produces important variations in cerebrospinal fluid proteins that could be due to a choroid plexus dysfunction and this fact supports the close connection between hypertension and blood to cerebrospinal fluid barrier disruption. 1. Introduction Cerebrospinal fluid is a functional system closely connected to the brain, and changes or variations in the CSF may mean an alteration in the brain expressed by encephalic disorders. However, the composition of CSF may also be altered by systemic diseases, such as arterial hypertension, and cerebral ventricular dilatation, changes in CSF protein, and variations of the choroid plexus and other circumventricular organs (CVO) have been described in spontaneously hypertensive rats (SHR) [1–5]. Therefore, SHR develop hydrocephalus and experimental studies explain that hydrocephalus induces alterations in CSF since there are disturbances, in the hydrocephalic brain, of oxidative metabolism and neurotransmission and perhaps damage to periventricular cells, particularly when intracranial pressure is elevated [6]. The sharp increase in systemic blood pressure only causes an acute increase in CSF pressure in normotensive animals and not in hypertensive patients [6]. The CSF pressure of SHR showed greater protection to the acute effects of phenylephrine than in control Wistar-Kyoto (WKY) rats, but a permeability increase of the blood to cerebrospinal fluid barrier to sucrose in
Cerebrospinal Fluid Concentration of Interleukin-6 and Interleukin-10 in Idiopathic Intracranial Hypertension
Hamed ReihaniKermani,Mohsen Soltani Gerd Faramarzi,Mehdi Ansari,Alireza Ghafarinejad
Journal of Medical Sciences , 2008,
Abstract: The aim of investigation was to determine interleukin-6 (IL-6; a proinflammatory cytokine) and IL-10 (an anti-inflammatory cytokine) concentrations in cerebrospinal fluid (CSF) of Idiopathic Intracranial Hypertension patients (IIH). The study covered 28 middle aged female (IIH patients, n = 14; controls, n = 14). CSF IL-6 and IL-10 concentration were determined by the use of commercial enzyme-linked immunosorbent assay (ELISA) kits. Concentration of IL-6 and IL-10 in CSF of IIH patients was 23.6±3.46 pg mL 1 and 3.7±0.5 pg mL 1 and in controls was 1.8±1.9 and 4.0±1.0 pg mL 1, respectively. Elevated IL-6 concentration in IIH patients found to be statistically significant in comparison to controls (p<0.05). There was no significant difference of IL-10 in IIH and controls. Role of immune system and inflammatory processes in etiology and pathogenesis of IIH must be taking into account.
Ocular Hypertension: General Characteristics and Estimated Cerebrospinal Fluid Pressure. The Beijing Eye Study 2011  [PDF]
Jost B. Jonas, Ningli Wang, Ya Xing Wang, Qi Sheng You, Diya Yang, Liang Xu
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0100533
Abstract: Purpose To examine characteristics of ocular hypertensive subjects and potential associations with estimated cerebrospinal fluid pressure (estCSFP). Methods The population-based Beijing Eye Study 2011 included 3468 individuals with a mean age of 64.6±9.8 years. Ocular hypertension was defined as intraocular pressure (IOP) >21 mmHg, normal optic nerve head appearance and normal retinal nerve fiber layer thickness. IOP was corrected for its dependence on central corneal thickness (CCT) and corneal curvature radius. Estimated CSFP was calculated as CSFP [mmHg] = 0.44×Body Mass Index [kg/m2]+0.16×Diastolic Blood Pressure [mmHg]?0.18×Age [Years]?1.91. Estimated trans-lamina cribrosa pressure difference (estTLCPD) was IOP–estCSFP. Results EstCSFP (10.5±3.6 mmHg versus 9.0±3.7 mmHg; P = 0.003) and estTLCPD (12.0±4.4 mmHg versus 5.4±3.8 mmHg; P<0.001) were higher in the ocular hypertensive group than in the normotensive group. In binary regression analysis, ocular hypertension was associated with increased estCSFP (P = 0.03; odds ratio (OR): 1.08; 95% confidence interval (CI): 1.01, 1.17) after adjusting for prevalence of arterial hypertension (P = 0.07; OR: 1.79; 95%CI: 0.96, 3.34), retinal nerve fiber layer thickness (P = 0.03; OR: 0.97; 95%CI: 0.95, 0.997) and blood glucose concentration (P = 0.006; OR: 1.17; 95%CI: 1.04, 1.30). Conclusions Ocular hypertensive subjects (with IOP correction for CCT and corneal curvature) as compared to ocular normotensive subjects had a significantly higher estCSFP in univariate analysis and in multivariate analysis. Despite of a higher estCSFP, estTLCPD was still markedly higher in ocular hypertensive eyes than in ocular normotensive eyes.
Cerebrospinal Fluid Diversion Procedures for Treatment of Idiopathic Intracranial Hypertension: Single Center Experience  [PDF]
Mahmoud M. Taha, Safwat Abouhashem, Ayman Abedelrahman
Open Journal of Modern Neurosurgery (OJMN) , 2017, DOI: 10.4236/ojmn.2017.73009
Abstract: Idiopathic intracranial hypertension (IIH) is a disorder characterized by increased intracranial pressure without any identifiable etiology with normal brain imaging and normal cerebrospinal fluid (CSF) content. CSF diversion procedures are commonly used for treatment if medical treatment failed. The aim of this study is to report our experience in treatment of IIH with lumboperitoneal (LP) and stereotactic guided ventriculoperitoneal (VP) shunts. The clinical data of 43 consecutive patients with IIH refractory to medical treatment and underwent CSF diversion procedures between 2009 and 2014 were analyzed. 29 patients underwent LP shunts and the remaining 14 patients underwent stereotactic guided Ventricular shunts. All patients underwent clinical, imaging and CSF manometry evaluation. 38 (88.4%) patients were female and the remaining 5 (11.6%) patients were male. The mean age was 27.2 years. The opening pressure was above 300 mm H2O in 26 (69.8%) patients. Headache (100%) and blurring and/or diminution of vision (81.4%) were the commonest clinical presentation. 36 (83.7%) patients reported recovery of their headache and 30 (69.7%) patients showed complete resolution of papilledema. The clinical outcome between both procedures was not significant. The incidence of perioperative complications (20.7% vs. 0%) and shunt revisions (27.6% vs. 7.1%) were higher in patients with LP shunt than patients with stereotactic Ventricular shunts. The results of this study demonstrate that both LP and Ventricular shunts are valid diversion procedures for treatment of IIH. Stereotactic guided Ventricular shunt has lower incidence of complications and revisions and seems to be safe, effective and feasible alternative procedure for treatment of IIH.
Protective Effects of Aliskiren, Enalapril and Valsartan on Hypertension Target Organs in Spontaneously Hypertensive Rats
Kalina Gjorgjievska,Maja Slaninka-Miceska,Gordana Petrusevska
Macedonian Journal of Medical Sciences , 2011,
Abstract: Aim: Aliskiren is the first orally active renin inhibitor approved for treatment of essential hypertension. There are as yet no clinical data regarding the ability of aliskiren to prevent clinical end-points or reduce end-organ damage over and above the presumed effects of blood pressure reduction. The aim of this study was to find out if aliskiren has a potential to improve renal function and if it has a protective effect on hypertension target organs (kidney, heart and aorta). Materials and Methods: The study was conducted on 64 SHR rats (male and female), 20 weeks old, weighing from 250-300 g. Animals were divided into 4 groups and treated with aliskiren (100 mg/kg bw/24 h), enalapril (10 mg/kg bw/24 h) and valsartan (10 mg/kg bw/24 h). Effects of investigated drugs were evaluated by urinalysis and histopathological analysis.Results: Diuresis was significantly increased in the group of animals treated with enalapril and valsartan. Effect on diuresis with aliskiren was mild and statistically insignificant. No significant difference in urine pH between treated and control group of SHR rats was noted. Albuminuria was decreased in animals treated with enalapril and valsartan. Aliskiren after 28 days of treatment had a statistically insignificant effect on albuminuria in SHR rats. Only certain changes of wall thickness of arteries and arterioles were noted that led to improved perfusion and function of the kidneys more pronounced in rats treated with valsartan and enalapril. Effects of aliskiren on target organs were inferior compared to valsartan and enalapril.Conclusion: In SHR experimental model aliskiren has minor effects on hypertension target organs when compared to enalapril and valsaratan.
A família do p53: aspectos estruturais e funcionais do p73 e do p63
Ribeiro-Silva, Alfredo;Zucoloto, Sérgio;
Jornal Brasileiro de Patologia e Medicina Laboratorial , 2003, DOI: 10.1590/S1676-24442003000200014
Abstract: the p53 gene has a key role in the cell cycle control. when mutated, it promotes the development of neoplasms, acting in so far as a tumor suppressor gene in normal conditions. recently, genes homologue to p53 were identified, named p73 e p63, probably originated from a common ancestral gene. despite the great structural homology, the members of p53 family have functional differences. this article aims to discourse about the major structural and functional aspects of p73 and p63, reinforcing their role in human tumorigenesis. p73 activates several p53 responsive genes and, when overexpressed, inhibits the p53 action. it is rarely mutated in neoplasms and its role in human tumorigenesis is still controversial. p63 is not a classical tumor suppressor gene, being essential for the maintenance of a population of precursor cells (stem cells) in several epithelial tissues. p63 is detectable in the basal cells of several epithelial organs like skin and prostate and could be considered a hallmark of cellular undifferentiation. p63 is a recently described marker and still requires more investigations to determine its role in the development of neoplasms in humans.
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