ABSTRACT
[Abstract] Oligodendroglial lineage cells (OLGs) are important cell reserves for myelination and remyelination. Recent studies of central nervous system (CNS) indicated that besides traditional CNS immune cells like microglia, primitive cells of oligodendroglial lineage, oligodendrocyte progenitor cells (OPCs) can also actively participate immune responses. Simulated by physiological or pathological factors, OPCs can express a series of receptors,signaling and/ or regulatory molecules et al, in this way,OPCs can play a critical role in both development and maintenance of the blood-cerebrospinal fluid barrier (BCB), and most essentially, in initial stage for recruitment of peripheral immune cells and initial immune activation. Besides, in neurological disorders, recent research has revealed that OPCs can transform to disease-specific cell states, characterized by activation of immune cell exclusive genes. These findings may provide the basis for a new insight into the therapeutic strategy of neuron disorders and neurovascular diseases by effectively regulating OPCs.
ABSTRACT
Introduction: Defining mechanisms governing the diffusion from blood to cerebrospinal fluid is central to understanding immune function in the central nervous system. Objective: To describe the dynamics of diffusion of the lectin pathway components from blood to cerebrospinal fluid. Methods: It was organized the information available in PubMed database and of papers from journals, and abstract books from international congresses belongs mainly to Cuban authors all about the lectin pathway of complement including manan-binding lectin (MBL) and ficolins complexed with the MBL-associated serine proteases (MASP2), and of other components like MASP3, Map44 as regulatory components and the different starters like MBL, ficolins and CLLK. Results: All the lectin pathways component are blood derived proteins but at the same time it could be synthesized intrathecally. Most of the protein can be transferred from blood to cerebrospinal fluid in different aggregation forms and some of them can be described as a consuming curve. The control mechanism of regulation the lectin pathway can be followed by molecules as MASP3 and Map44. Conclusions: The under- constructed lectin pathway of the complement system required not only the available information in different journals. It had to be completed by reviewing the congress abstract book and congress website of the last years(AU)
Subject(s)
Humans , Cerebrospinal Fluid/physiologyABSTRACT
INTRODUCCIÓN: la dinámica particular de las proteínas derivadas del cerebro en el líquido cefalorraquídeo es diferente a la dinámica de las proteínas derivadas de la sangre. OBJETIVO: describir los datos empíricos de la lectina de unión a manosa y brindar una interpretación teórica de la dinámica de esta proteína a través de la confección un nuevo reibergrama. MÉTODOS: la lectina de unión a manosa en suero y líquido cfalorraquídeo, fue medida en 40 adultos normales a través de un ensayo inmunofluorométrico. El criterio diagnóstico estuvo basado en; muestras controles (pacientes normales) y muestras de pacientes con enfermedades que cursaron con disfunción de barrera sangre-líquido cefalorraquídeo. RESULTADOS: el coeficiente de correlación entre la lectina de unión a manosa en el líquido cefalorraquídeo y en el suero, fue muy bajo. El reibergrama de la lectina de unión a manosa se diseñó de acuerdo con procedimientos previos. CONCLUSIONES: bajo cualquier condición de barrera sangre-líquido cefalorraquídeo, el reibergrama puede identificar la ocurrencia de síntesis intratecal de lectina de unión a manosa.
BACKGROUND: The dynamics of brain derived proteins in cerebrospinal fluid is different from the dynamics of blood-derived proteins. Aim: To describe the empirical data for mannan binding lectin and gives a theoretical interpretation of the dynamics of this protein in cerebrospinal fluid through a new reibergram. METHODS: Serum and cerebrospinal fluid mannan binding lectin were measured in 40 normal adults by immunofluorometric assays. The diagnostic criteria were based in; normal control samples defined clinically and diseases with blood-cerebrospinal fluid barrier dysfunction. RESULTS: Correlation coefficient between cerebrospinal fluid MBL and serum MBL was very low. Mannan binding lectin reibergram was designed according with previous procedures. CONCLUSION: Under all conditions of the blood-cerebrospinal fluid barrier, the reibergram can identify the occurrence of intrathecal mannan binding lectin synthesis.
Subject(s)
Fluoroimmunoassay/methods , Cerebrospinal Fluid Proteins/analysis , Mannose-Binding Lectin , Software Design , Informed ConsentABSTRACT
OBJECTIVE To investigate the effects of lead exposure on the permeability,secretion and transportation function of blood-cerebro-spinal fluid barrier (BCB)of rats in order to provide the theo-rical basis for elucidating the mechanis m of lead induced neurotoxicity.MEHTODS 60 SPF SD rats were rando mly divided into 4 groups,including a control group and three doses lead exposed groups. Rat in the lead exposure groups were given drinking water containning 0.05%,0.1 % and 0.2% lead acetate (at dose of 80,160,320 mg·kg -1 )for 8 weeks.Laser scanning confocal microscopy was uti-lized to determine the lead content in seru m,cerebrospinal fluid (CSF)and choroid plexus sa mples. Morris maze was used to test learning and me mory.Fe moral artery perfusion of Evans blue (EB)and fluorescein sodiu m (NaFI)was performed to measure BCB permeability function.Confocal laser scan-ning was applied to detect junction adhesion molecule (JAM)and occludin protein expression in choroid plexus.ELISA was used to measure the concentration of transthyretin (TTR)and leptin in seru m and CSF.RESULTS The lead content in seru m,choroid plexus and CSF significantly increased,especially the lead level in CSF.Morris water maze data showed that escape latency of rat in lead acetate 160 and 320 mg·kg -1 group were 52 ±12,(89 ±19)s,respectively,longer than that of control group 〔(28 ±7)s, P<0.05〕.The ti mes across platform of rats in lead acetate 160 and 320 mg·kg -1 group were lower than that of control group(P <0.05).The NaFI content in CSF of rats in all lead acetate exposure groups were 0.94 ±0.09,1 .02 ±0.03 and (1 .08 ±0.18)mg·L -1 ,respectively,and were higher than those of control group〔(0.74 ±0.04)mg·L -1 〕;While the EB content in CSF of rat in lead acetate 160 and 320 mg·kg -1 group were higher than the control group(P <0.05),which indicated that lead acetate exposure at low dose can lead to the increase of permeability of BCB.Laser scanning confocal micro-scope i mages showed that the JAM protein expression of choroid plexus in lead acetate 160 and 320 mg·kg -1 group were 44.9% and 42.9% of the control group.Sa me decline was seen in terms of occludin expression.The TTR content of CSF of rats in lead acetate 80 mg·kg -1 group was (32.3 ± 1 1 .7)ng·g -1 protein,lower than that of the control group,and the difference was significant.This decline was also noted in lead acetate 160 and 320 mg·kg -1 group.The data of TTR in CSF suggested that the low dose lead acetate exposure can disrupt the BCB secretion function.The leptin levels in CSF of lead acetate 160 and 320 mg·kg -1 group were lower than that in the control group (P <0.05 ). CONCLUSION Lead exposure did disrupt the permeability,transportation and secretion function of BCB.Our data suggest that BCB dysfunction might be involved in the mechanis m of lead induced neurotoxicity.