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1.
Diagn Microbiol Infect Dis ; 100(4): 115403, 2021 Aug.
Article in English | MEDLINE | ID: mdl-34058541

ABSTRACT

Since the worldwide outbreak of the novel coronavirus (SARS-CoV-2), the question raised whether infected patients would elicit long-lasting protective immunity. Several companies developed serological assays for the detection of SARS-CoV-2 antibodies. In this study, we compared 4 different serology assays in convalescents up to 7 months post-infection. Both Abbott assays showed a significative decrease of IgG antibodies over time. Whereas the Elecsys Anti­SARS­CoV­2 N assay (Roche) initially showed a significant increase, antibody titers significantly decreased at the latest timepoint. Although not significant, the Elecsys Anti­SARS­CoV­2 S assay (Roche) showed tendency towards increasing titers overtime. Our data showed that results of SARS-CoV-2 serology should be interpreted with caution.


Subject(s)
Antibodies, Viral/blood , COVID-19 Serological Testing/methods , COVID-19/blood , Immunoglobulin G/blood , SARS-CoV-2/immunology , Antibodies, Viral/metabolism , COVID-19/immunology , Humans , Immunoglobulin G/metabolism , Sensitivity and Specificity , Time Factors
2.
Microb Drug Resist ; 22(2): 134-6, 2016 Mar.
Article in English | MEDLINE | ID: mdl-26954370

ABSTRACT

We reported a woman with urinary-tract infection caused by OXA-48 producing Klebsiella pneumoniae. Using molecular techniques, we showed that she might acquire this bacterium from another family member who lived in the same house. The two isolates, although different by pulsed-field gel electrophoresis and multilocus sequence typing, carried blaOXA-48 in a similar IncL/M plasmid. This case report shows that community spreading of carbapenemase producing Enterobacteriaceae occurs in the low endemic area not only in nosocomial setting but also in the community.


Subject(s)
Anti-Bacterial Agents/pharmacology , DNA, Bacterial/genetics , Drug Resistance, Multiple, Bacterial/genetics , Klebsiella pneumoniae/genetics , Plasmids/metabolism , beta-Lactamases/genetics , Adolescent , Belgium , Carbapenems/pharmacology , Community-Acquired Infections , Electrophoresis, Gel, Pulsed-Field , Family Characteristics , Female , Gene Expression , Humans , Klebsiella Infections/drug therapy , Klebsiella Infections/microbiology , Klebsiella pneumoniae/drug effects , Klebsiella pneumoniae/enzymology , Klebsiella pneumoniae/isolation & purification , Microbial Sensitivity Tests , Multilocus Sequence Typing , Plasmids/chemistry , Sequence Analysis, DNA , beta-Lactamases/metabolism
3.
Nutr Neurosci ; 16(2): 78-82, 2013 Mar.
Article in English | MEDLINE | ID: mdl-23324588

ABSTRACT

L-Theanine, an ethylamide derivate of glutamate found in abundance in green tea, has been shown to exert beneficial actions in animal models for several neurological disorders. We here investigated for the first time the effect of L-theanine intake on seizure susceptibility using acute pilocarpine and pentylenetetrazol (PTZ) mouse models for studying, respectively, limbic seizures or primarily generalized seizures. Moreover, we studied the effect of l-theanine intake on extracellular hippocampal and cortical glutamate and gamma-aminobutyric acid (GABA) levels, using in vivo microdialysis. Feeding mice with a 4% L-theanine solution significantly decreased their susceptibility to pilocarpine-induced seizures whereas susceptibility to PTZ-induced seizures was increased. The latter effect was linked to decreased extracellular GABA concentrations in frontal cortex.


Subject(s)
Glutamates/pharmacology , Seizures/drug therapy , gamma-Aminobutyric Acid/metabolism , Animals , Disease Models, Animal , GABA Agents/metabolism , Glutamates/administration & dosage , Glutamic Acid/metabolism , Hippocampus/drug effects , Hippocampus/metabolism , Male , Mice , Mice, Inbred Strains , Microdialysis , Pentylenetetrazole/adverse effects , Pilocarpine/adverse effects , Seizures/chemically induced , Tea/chemistry
4.
Neurotherapeutics ; 9(3): 658-72, 2012 Jul.
Article in English | MEDLINE | ID: mdl-22669710

ABSTRACT

Ghrelin is a pleiotropic neuropeptide that has been recently implicated in epilepsy. Animal studies performed to date indicate that ghrelin has anticonvulsant properties; however, its mechanism of anticonvulsant action is unknown. Here we show that the anticonvulsant effects of ghrelin are mediated via the growth hormone secretagogue receptor (GHSR). To our surprise, however, we found that the GHSR knockout mice had a higher seizure threshold than their wild-type littermates when treated with pilocarpine. Using both in vivo and in vitro models, we further discovered that inverse agonism and desensitization/internalization of the GHSR attenuate limbic seizures in rats and epileptiform activity in hippocampal slices. This constitutes a novel mechanism of anticonvulsant action, whereby an endogenous agonist reduces the activity of a constitutively active receptor.


Subject(s)
Anticonvulsants/therapeutic use , Ghrelin/therapeutic use , Limbic System/drug effects , Receptors, Ghrelin/metabolism , Seizures/drug therapy , Seizures/pathology , Analysis of Variance , Animals , Anticonvulsants/pharmacology , Calcium/metabolism , Disease Models, Animal , Disease Susceptibility , Dose-Response Relationship, Drug , Drug Interactions , Electric Stimulation , Excitatory Postsynaptic Potentials/drug effects , Excitatory Postsynaptic Potentials/genetics , Green Fluorescent Proteins/genetics , HEK293 Cells , Hippocampus/cytology , Humans , In Vitro Techniques , Limbic System/physiopathology , Male , Mice , Mice, Inbred C57BL , Mice, Knockout , Microdialysis , Muscarinic Agonists/toxicity , Neurons/drug effects , Patch-Clamp Techniques , Pilocarpine/toxicity , Piperidines/therapeutic use , Pyrazoles/therapeutic use , Rats , Rats, Wistar , Receptors, Ghrelin/agonists , Receptors, Ghrelin/deficiency , Seizures/genetics , Severity of Illness Index , Species Specificity , Transfection , gamma-Aminobutyric Acid/metabolism
5.
Epilepsy Behav ; 22(3): 450-60, 2011 Nov.
Article in English | MEDLINE | ID: mdl-21962757

ABSTRACT

In the past, antidepressants have been thought to possess proconvulsant properties. This assumption remains controversial, however, because anticonvulsant effects have been attributed to certain antidepressants. To date, it remains unclear which antidepressants can be used for the treatment of patients with epilepsy with depression. The present study was designed to determine the anticonvulsant and/or proconvulsant effects of three antidepressants (citalopram, reboxetine, bupropion) against pilocarpine- and pentylenetetrazole-induced acute seizures in larval zebrafish and mice. In zebrafish, all antidepressants were anticonvulsant in the pentylenetetrazole model. In addition, citalopram was anticonvulsant in the zebrafish pilocarpine model, whereas reboxetine and bupropion were without significant effect. In mice all three antidepressants increased some thresholds for pentylenetetrazole-induced convulsive-like behaviors at varying doses, whereas thresholds for pilocarpine-induced convulsive-like behaviors were generally lowered, particularly at the highest doses tested. In general we conclude that the convulsant liability of antidepressants is model and concentration dependent.


Subject(s)
Antidepressive Agents/therapeutic use , Convulsants/toxicity , Seizures/chemically induced , Seizures/drug therapy , Analysis of Variance , Animals , Animals, Genetically Modified , Behavior, Animal/drug effects , Disease Models, Animal , Dose-Response Relationship, Drug , Drug Interactions , Green Fluorescent Proteins/genetics , Male , Mice , Pentylenetetrazole/toxicity , Pilocarpine/toxicity , Seizures/mortality , Seizures/physiopathology , Zebrafish
6.
J Neurosci ; 31(15): 5792-803, 2011 Apr 13.
Article in English | MEDLINE | ID: mdl-21490221

ABSTRACT

System x(c)- exchanges intracellular glutamate for extracellular cystine, giving it a potential role in intracellular glutathione synthesis and nonvesicular glutamate release. We report that mice lacking the specific xCT subunit of system x(c)- (xCT(-/-)) do not have a lower hippocampal glutathione content, increased oxidative stress or brain atrophy, nor exacerbated spatial reference memory deficits with aging. Together these results indicate that loss of system x(c)- does not induce oxidative stress in vivo. Young xCT(-/-) mice did however display a spatial working memory deficit. Interestingly, we observed significantly lower extracellular hippocampal glutamate concentrations in xCT(-/-) mice compared to wild-type littermates. Moreover, intrahippocampal perfusion with system x(c)- inhibitors lowered extracellular glutamate, whereas the system x(c)- activator N-acetylcysteine elevated extracellular glutamate in the rat hippocampus. This indicates that system x(c)- may be an interesting target for pathologies associated with excessive extracellular glutamate release in the hippocampus. Correspondingly, xCT deletion in mice elevated the threshold for limbic seizures and abolished the proconvulsive effects of N-acetylcysteine. These novel findings sustain that system x(c)-) is an important source of extracellular glutamate in the hippocampus. System x(c)(-) is required for optimal spatial working memory, but its inactivation is clearly beneficial to decrease susceptibility for limbic epileptic seizures.


Subject(s)
Amino Acid Transport System y+/physiology , Extracellular Space/metabolism , Glutamic Acid/metabolism , Hippocampus/physiology , Limbic System/physiology , Memory, Short-Term/physiology , Oxidative Stress/physiology , Seizures/physiopathology , Space Perception/physiology , Animals , Blotting, Western , Brain/anatomy & histology , DNA/genetics , Electroencephalography , Genotype , Glutathione/metabolism , Immunohistochemistry , Male , Maze Learning/physiology , Mice , Mice, Inbred C57BL , Mice, Knockout , Microdialysis , Motor Activity/physiology , Neuroglia/physiology , Psychomotor Performance/physiology , Rats , Rats, Wistar , Reverse Transcriptase Polymerase Chain Reaction , Seizures/chemically induced , Seizures/genetics
7.
J Alzheimers Dis ; 24(2): 287-300, 2011.
Article in English | MEDLINE | ID: mdl-21297271

ABSTRACT

Using 8- and 18-month-old AßPP23 mice, we investigated the involvement of high-affinity glutamate transporters (GLAST, GLT-1, EAAC1), vesicular glutamate transporters (VGLUT1-3) and xCT, the specific subunit of system x(c)⁻, in Alzheimer's disease (AD) pathogenesis. Transporter expression was studied in cortical and hippocampal tissue and linked to extracellular glutamate and glutamate reuptake activity as measured using in vivo microdialysis. In 8-month-old animals, we could not observe plaque formation or gliosis. Yet, in hippocampus as well as cortex GLAST and GLT-1 expression was decreased. Whereas in cortex this was accompanied by upregulated VGLUT1 expression, extracellular glutamate concentrations were decreased. Surprisingly, inhibiting glutamate reuptake with TBOA revealed increased glutamate reuptake activity in cortex of AßPP23 mice, despite decreased GLAST and GLT-1 expression, and resulted in status epilepticus in all AßPP23 mice, contrary to wildtype littermates. In hippocampus of 8-month-old AßPP23 mice, we observed increased EAAC1 expression besides the decrease in GLAST and GLT-1. Yet, glutamate reuptake activity was drastically decreased according to the decreased GLAST and GLT-1 expression. In 18-month-old AßPP23 mice, plaque formation and gliosis in cortex and hippocampus were accompanied by decreased GLT-1 expression. We also showed, for the first time, increased cortical expression of VGLUT3 and xCT together with a strong tendency towards increased cortical extracellular glutamate levels. VGLUT2 expression remained unaltered in all conditions. The present findings support the hypothesis that alterations in transport of glutamate, and more particular via GLT-1, may be involved in AD pathogenesis.


Subject(s)
Aging , Alzheimer Disease/metabolism , Alzheimer Disease/pathology , Amino Acid Transport System X-AG/metabolism , Cerebral Cortex/metabolism , Hippocampus/metabolism , Alzheimer Disease/genetics , Amino Acid Transport System X-AG/classification , Amyloid beta-Peptides/metabolism , Amyloid beta-Protein Precursor/genetics , Animals , Chromatography, High Pressure Liquid , Disease Models, Animal , Excitatory Amino Acid Transporter 2/genetics , Excitatory Amino Acid Transporter 2/metabolism , Gene Expression Regulation/genetics , Glutamic Acid , Humans , Mice , Mice, Transgenic , Mutation/genetics
8.
FASEB J ; 25(4): 1359-69, 2011 Apr.
Article in English | MEDLINE | ID: mdl-21191088

ABSTRACT

Malfunctioning of system x(c)(-), responsible for exchanging intracellular glutamate for extracellular cystine, can cause oxidative stress and excitotoxicity, both important phenomena in the pathogenesis of Parkinson's disease (PD). We used mice lacking xCT (xCT(-/-) mice), the specific subunit of system x(c)(-), to investigate the involvement of this antiporter in PD. Although cystine that is imported via system x(c)(-) is reduced to cysteine, the rate-limiting substrate in the synthesis of glutathione, deletion of xCT did not result in decreased glutathione levels in striatum. Accordingly, no signs of increased oxidative stress could be observed in striatum or substantia nigra of xCT(-/-) mice. In sharp contrast to expectations, xCT(-/-) mice were less susceptible to 6-hydroxydopamine (6-OHDA)-induced neurodegeneration in the substantia nigra pars compacta compared to their age-matched wild-type littermates. This reduced sensitivity to a PD-inducing toxin might be related to the decrease of 70% in striatal extracellular glutamate levels that was observed in mice lacking xCT. The current data point toward system x(c)(-) as a possible target for the development of new pharmacotherapies for the treatment of PD and emphasize the need to continue the search for specific ligands for system x(c)(-).


Subject(s)
Amino Acid Transport System y+/deficiency , Dopamine/physiology , Neurons/drug effects , Oxidopamine/toxicity , Aging/physiology , Amino Acid Transport System y+/physiology , Animals , Corpus Striatum/metabolism , Cystine/metabolism , Glioma/metabolism , Glutamic Acid/metabolism , Glutathione/metabolism , Mice , Mice, Knockout , Neurodegenerative Diseases/prevention & control , Neurons/metabolism , Substantia Nigra/metabolism , Tumor Cells, Cultured
9.
Neurochem Int ; 57(5): 572-8, 2010 Nov.
Article in English | MEDLINE | ID: mdl-20643175

ABSTRACT

Striatal dopamine loss in Parkinson's disease is accompanied by a dysregulation of corticostriatal glutamatergic neurotransmission. Within this study, we investigated striatal expression and activity of the glial high-affinity Na(+)/K(+)-dependent glutamate transporters, GLT-1 and GLAST, in the 6-hydroxydopamine hemi-Parkinson rat model at different time points after unilateral 6-hydroxydopamine injection into the medial forebrain bundle. Using semi-quantitative Western blotting and an ex vivo D-[(3)H]-aspartate uptake assay, we showed a time-dependent bilateral effect of unilateral 6-hydroxydopamine lesioning on the expression as well as activity of GLT-1. At 3 and 12 weeks post-lesion, striatal GLT-1 function was bilaterally upregulated whereas at 5 weeks there was no change. Even though our data do not allow a straightforward conclusion as for the role of glutamate transporters in the pathogenesis of the disease, they do clearly demonstrate a link between disturbed glutamatergic neurotransmission and glutamate transporter functioning in the striatum of a rat model for Parkinson's disease.


Subject(s)
Corpus Striatum/physiology , Excitatory Amino Acid Transporter 2/physiology , Parkinson Disease, Secondary/physiopathology , Animals , Aspartic Acid/metabolism , Blotting, Western , Chromatography, High Pressure Liquid , Corpus Striatum/metabolism , Dopamine/metabolism , Excitatory Amino Acid Transporter 1/biosynthesis , Excitatory Amino Acid Transporter 1/genetics , Excitatory Amino Acid Transporter 2/biosynthesis , Excitatory Amino Acid Transporter 2/genetics , Immunohistochemistry , Medial Forebrain Bundle/metabolism , Medial Forebrain Bundle/physiology , Oxidopamine , Parkinson Disease, Secondary/chemically induced , Piperazines/metabolism , Rats , Synaptosomes/metabolism , Time Factors
10.
Neurochem Int ; 57(2): 111-8, 2010 Sep.
Article in English | MEDLINE | ID: mdl-20450947

ABSTRACT

Parkinson's disease is characterized by disturbed glutamatergic neurotransmission in the striatum. Important mediators of extracellular glutamate levels are the vesicular glutamate transporters VGLUT1 and VGLUT2 in respectively corticostriatal and thalamostriatal afferents, next to the high-affinity Na(+)/K(+)-dependent glutamate transporters and the cystine/glutamate antiporter. In the present study, we compared bilateral striatal VGLUT1 and VGLUT2 protein expression as well as VGLUT1 and VGLUT2 transcript levels in the neocortex and parafascicular nucleus of hemi-Parkinson rats at different time intervals post unilateral 6-OHDA injection into the medial forebrain bundle versus controls. Three weeks post-injection we detected increased striatal VGLUT1 expression together with decreased VGLUT2 expression. On the other hand, after twelve weeks, the expression of VGLUT1 was decreased in hemi-Parkinson rats whereas the striatal expression of VGLUT2 was comparable to control rats. No effect could be seen on VGLUT transcript levels in the respective projection areas at any time. In conclusion, we observed a biphasic and bilateral change in the protein expression levels of both VGLUTs in the striatum of hemi-Parkinson rats indicative for a different and time-dependent change in glutamatergic neurotransmission from the two types of striatal afferents.


Subject(s)
Corpus Striatum/metabolism , Parkinson Disease/metabolism , Vesicular Glutamate Transport Protein 1/metabolism , Vesicular Glutamate Transport Protein 2/metabolism , Animals , Base Sequence , Blotting, Western , DNA Primers , Disease Models, Animal , In Situ Hybridization , Rats
11.
Neurochem Int ; 55(1-3): 41-4, 2009.
Article in English | MEDLINE | ID: mdl-19171171

ABSTRACT

Glutamate, the most abundant excitatory neurotransmitter in the central nervous system, is well known to be implicated in epileptic seizures. Therefore, impairments in glutamate transport could have an involvement in the mechanism of epileptogenesis. The uptake of glutamate into synaptic vesicles is mediated by vesicular glutamate transporters (vGLUTs). There are three known vGLUT isoforms, vGLUT1-3. In this study, we are particularly interested in the vGLUT2 isoform. We investigated the possible role of vGLUT2 in pentylenetetrazol (PTZ)-induced seizure generation. Seizure threshold of PTZ was compared in vGLUT2 heterozygous knock out (HET) and wild type (WT) mice. In comparison with their WT littermates a lower dose of PTZ was needed in the vGLUT2 HET mice until the onset of the first myoclonic jerk. The threshold for PTZ-induced clonic seizure activity was also lower in the vGLUT2 HET mice. These results indicate, for the first time, that vGLUT2 is likely involved in the epileptogenesis of generalized seizures.


Subject(s)
Epilepsy, Tonic-Clonic/chemically induced , Epilepsy, Tonic-Clonic/genetics , Seizures/chemically induced , Seizures/genetics , Vesicular Glutamate Transport Protein 2/genetics , Animals , Cerebral Cortex/drug effects , Cerebral Cortex/physiology , Convulsants , Electroencephalography , Epilepsy, Generalized/chemically induced , Epilepsy, Generalized/genetics , Heterozygote , Male , Mice , Mice, Knockout , Neural Pathways/drug effects , Neural Pathways/physiology , Pentylenetetrazole , Telemetry , Thalamus/drug effects , Thalamus/physiology
12.
Neuroreport ; 19(16): 1589-92, 2008 Oct 29.
Article in English | MEDLINE | ID: mdl-18806690

ABSTRACT

Altered glutamate signaling is associated with Parkinson's disease. To study the involvement of the cystine/glutamate antiporter in the pathogenesis of Parkinson's disease, we developed new polyclonal antibodies recognizing xCT, the specific subunit of this antiporter. The striatal xCT protein expression level was investigated in a hemi-Parkinson rat model, using semiquantitative western blotting. We observed time-dependent changes after a unilateral 6-hydroxydopamine lesion of the nigrostriatal pathway with increased expression levels in the deafferented striatum after 3 weeks. Twelve weeks postlesion, expression levels returned to normal. These data suggest, for the first time, an involvement of the cystine/glutamate antiporter in determining the aberrant glutamate neurotransmission in the striatum of a parkinsonian brain.


Subject(s)
Amino Acid Transport System y+/metabolism , Corpus Striatum/metabolism , Parkinson Disease, Secondary/metabolism , Substantia Nigra/metabolism , Animals , Blotting, Western , Corpus Striatum/drug effects , Disease Models, Animal , Enzyme-Linked Immunosorbent Assay , Injections, Intraperitoneal , Male , Medial Forebrain Bundle/drug effects , Medial Forebrain Bundle/metabolism , Medial Forebrain Bundle/pathology , Mice , Mice, Knockout , Oxidopamine/administration & dosage , Oxidopamine/toxicity , Parkinson Disease, Secondary/chemically induced , Parkinson Disease, Secondary/pathology , Rabbits , Rats , Rats, Wistar , Substantia Nigra/drug effects , Time Factors
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