13 results on '"Mailleux J"'
Search Results
2. The phosphodiesterase 4 (PDE4) inhibitor roflumilast improves remyelination in a mouse model for multiple sclerosis
- Author
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Schepers, M., Mailleux, J., Bogie, J., Goethem, N., Hellings, N., Jerome Hendriks, Prickaerts, J., and Vanmierlo, T.
3. Development, Validation, and Implementation of an Augmented Multiwell, Multitarget Quantitative PCR for the Analysis of Human Papillomavirus Genotyping through Software Automation, Data Science, and Artificial Intelligence.
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Pereira AR, Redzic N, Van Vooren S, Pelak K, Broekmans A, Desloovere G, Vanden Broeck D, Kehoe K, Bogers J, Coppens A, Vreysen S, Mailleux J, and Uten W
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- Humans, Female, Genotype, Uterine Cervical Neoplasms virology, Uterine Cervical Neoplasms diagnosis, Viral Load methods, Genotyping Techniques methods, Reproducibility of Results, DNA, Viral genetics, Human Papillomavirus Viruses, Papillomaviridae genetics, Software, Artificial Intelligence, Real-Time Polymerase Chain Reaction methods, Papillomavirus Infections diagnosis, Papillomavirus Infections virology
- Abstract
The value of human papillomavirus (HPV) testing for cervical cancer screening is well established; however, its use as a primary screening option or as a reflex test after atypical cytology results is now gaining wider acceptance. The importance of full genotyping and viral load determination has been demonstrated to enhance the clinical understanding of the viral infection progression during follow-up or after treatment, thereby providing clinicians with supplementary tools for optimized patient management. We developed a new analysis method for the RIATOL quantitative PCR assay, and validated and implemented it in the laboratory of clinical molecular pathology at Algemeen Medisch Laboratorium (AML), under national accreditation and following the International Organization for Standardization guidelines. This study presents the successful validation of a high-throughput, multitarget HPV analysis method, with enhanced accuracy on both qualitative and quantitative end results. This is achieved by software standardization and automation of PCR curve analysis and interpretation, using data science and artificial intelligence. Moreover, the user-centric functionality of the platform was demonstrated to enhance both staff training and routine analysis workflows, thereby saving time and laboratory personnel resources. Overall, the integration of the FastFinder plugin semi-automatic analysis algorithm with the RIATOL real-time quantitative PCR assay proved to be a remarkable advancement in high-throughput HPV quantification, with demonstrated capability to provide highly accurate clinical-grade results and to reduce manual variability and analysis time., (Copyright © 2024 Association for Molecular Pathology and American Society for Investigative Pathology. All rights reserved.)
- Published
- 2024
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4. Liver X receptor beta deficiency attenuates autoimmune-associated neuroinflammation in a T cell-dependent manner.
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Bogie JFJ, Vanmierlo T, Vanmol J, Timmermans S, Mailleux J, Nelissen K, Wijnands E, Wouters K, Stinissen P, Gustafsson JÅ, Steffensen KR, Mulder M, Zelcer N, and Hendriks JJA
- Subjects
- Animals, Autoimmunity, Cholesterol metabolism, Disease Models, Animal, Humans, Liver X Receptors genetics, Mice, Mice, Inbred C57BL, Mice, Knockout, Neurogenic Inflammation, Encephalomyelitis, Autoimmune, Experimental immunology, Liver X Receptors metabolism, Microglia pathology, Multiple Sclerosis immunology, T-Lymphocytes immunology
- Abstract
The initiation and progression of autoimmune disorders such as multiple sclerosis (MS) is linked to aberrant cholesterol metabolism and overt inflammation. Liver X receptors (LXR) are nuclear receptors that function at the crossroads of cholesterol metabolism and immunity, and their activation is considered a promising therapeutic strategy to attenuate autoimmunity. However, despite clear functional heterogeneity and cell-specific expression profiles, the impact of the individual LXR isoforms on autoimmunity remains poorly understood. Here, we show that LXRα and LXRβ have an opposite impact on immune cell function and disease severity in the experimental autoimmune encephalomyelitis model, an experimental MS model. While Lxrα deficiency aggravated disease pathology and severity, absence of Lxrβ was protective. Guided by flow cytometry and by using cell-specific knockout models, reduced disease severity in Lxrβ-deficient mice was primarily attributed to changes in peripheral T cell physiology and occurred independent from alterations in microglia function. Collectively, our findings indicate that LXR isoforms play functionally non-redundant roles in autoimmunity, potentially having broad implications for the development of LXR-based therapeutic strategies aimed at dampening autoimmunity and neuroinflammation., (Copyright © 2021 Elsevier Ltd. All rights reserved.)
- Published
- 2021
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5. Stearoyl-CoA desaturase-1 impairs the reparative properties of macrophages and microglia in the brain.
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Bogie JFJ, Grajchen E, Wouters E, Corrales AG, Dierckx T, Vanherle S, Mailleux J, Gervois P, Wolfs E, Dehairs J, Van Broeckhoven J, Bowman AP, Lambrichts I, Gustafsson JÅ, Remaley AT, Mulder M, Swinnen JV, Haidar M, Ellis SR, Ntambi JM, Zelcer N, and Hendriks JJA
- Subjects
- ATP Binding Cassette Transporter 1 metabolism, Animals, Cell Line, Cholesterol metabolism, Endocytosis, Fatty Acids metabolism, Foam Cells metabolism, Humans, Inflammation pathology, Macrophages metabolism, Macrophages ultrastructure, Mice, Microglia metabolism, Myelin Sheath metabolism, Phagocytes pathology, Phagocytes ultrastructure, Phenotype, Protein Kinase C-delta metabolism, Stearoyl-CoA Desaturase deficiency, Brain pathology, Macrophages enzymology, Microglia enzymology, Stearoyl-CoA Desaturase metabolism
- Abstract
Failure of remyelination underlies the progressive nature of demyelinating diseases such as multiple sclerosis. Macrophages and microglia are crucially involved in the formation and repair of demyelinated lesions. Here we show that myelin uptake temporarily skewed these phagocytes toward a disease-resolving phenotype, while sustained intracellular accumulation of myelin induced a lesion-promoting phenotype. This phenotypic shift was controlled by stearoyl-CoA desaturase-1 (SCD1), an enzyme responsible for the desaturation of saturated fatty acids. Monounsaturated fatty acids generated by SCD1 reduced the surface abundance of the cholesterol efflux transporter ABCA1, which in turn promoted lipid accumulation and induced an inflammatory phagocyte phenotype. Pharmacological inhibition or phagocyte-specific deficiency of Scd1 accelerated remyelination ex vivo and in vivo. These findings identify SCD1 as a novel therapeutic target to promote remyelination., Competing Interests: Disclosures: The authors declare no competing interests exist., (© 2020 Bogie et al.)
- Published
- 2020
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6. Active liver X receptor signaling in phagocytes in multiple sclerosis lesions.
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Mailleux J, Vanmierlo T, Bogie JF, Wouters E, Lütjohann D, Hendriks JJ, and van Horssen J
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- Cells, Cultured, Humans, Multiple Sclerosis, Brain immunology, Brain metabolism, Liver X Receptors metabolism, Macrophages immunology, Macrophages metabolism, Myelin Sheath metabolism, Signal Transduction, Tissue Banks
- Abstract
Objective: We sought to determine the liver X receptor (LXR) ligands present in human macrophages after myelin phagocytosis and whether LXRs are activated in multiple sclerosis (MS) lesions., Methods: We used real-time quantitative polymerase chain reaction (PCR) and immunohistochemistry to determine expression of LXRs and their response genes in human phagocytes after myelin phagocytosis and in active MS lesions. We used gas chromatographic/mass spectrometric analysis to determine LXR-activating oxysterols and cholesterol precursors present and formed in myelin and myelin-incubated cells, respectively., Results: Myelin induced LXR response genes ABCA1 and ABCG1 in human monocyte-derived macrophages. In active MS lesions, we found that both gene expression and protein levels of ABCA1 and apolipoprotein E ( APOE) are upregulated in foamy phagocytes. Moreover, we found that the LXR ligand 27-hydroxycholesterol (27OHC) is significantly increased in human monocyte-derived macrophages after myelin uptake., Conclusion: LXR response genes are upregulated in phagocytes present in active MS lesions, indicating that LXRs are activated in actively demyelinating phagocytes. In addition, we have shown that myelin contains LXR ligands and that 27OHC is generated in human monocyte-derived macrophages after myelin processing. This suggests that LXRs in phagocytes in active MS lesions are activated at least partially by (oxy)sterols present in myelin and the generation thereof during myelin processing.
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- 2018
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7. Targeting demyelination via α-secretases promoting sAPPα release to enhance remyelination in central nervous system.
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Llufriu-Dabén G, Carrete A, Chierto E, Mailleux J, Camand E, Simon A, Vanmierlo T, Rose C, Allinquant B, Hendriks JJA, Massaad C, Meffre D, and Jafarian-Tehrani M
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- Amyloid Precursor Protein Secretases antagonists & inhibitors, Animals, Axons drug effects, Axons metabolism, Brain drug effects, Cells, Cultured, Cerebellum drug effects, Cerebellum metabolism, Corpus Callosum drug effects, Corpus Callosum metabolism, Corpus Callosum ultrastructure, Cuprizone administration & dosage, Demyelinating Diseases chemically induced, Demyelinating Diseases prevention & control, Lysophosphatidylcholines administration & dosage, Male, Mice, Inbred C57BL, Myelin Sheath drug effects, Myelin Sheath ultrastructure, Amyloid Precursor Protein Secretases metabolism, Amyloid beta-Protein Precursor metabolism, Brain metabolism, Demyelinating Diseases metabolism, Etazolate administration & dosage, Myelin Sheath metabolism, Neuroprotective Agents administration & dosage, Remyelination
- Abstract
Remyelination is an endogenous regenerative process of myelin repair in the central nervous system (CNS) with limited efficacy in demyelinating disorders. As strategies enhancing endogenous remyelination become a therapeutic challenge, we have focused our study on α-secretase-induced sAPPα release, a soluble endogenous protein with neuroprotective and neurotrophic properties. However, the role of sAPPα in remyelination is not known. Therefore, we investigated the remyelination potential of α-secretase-induced sAPPα release following CNS demyelination in mice. Acute demyelination was induced by feeding mice with cuprizone (CPZ) for 5weeks. To test the protective effect and the remyelination potential of etazolate, an α-secretase activator, we designed two treatment protocols. Etazolate was administrated either during the last two weeks or at the end of the CPZ intoxication. In both protocols, etazolate restored the number of myelinated axons in corpus callosum with a corresponding increase in the amount of MBP, one of the major myelin proteins in the brain. We also performed ex vivo studies to decipher etazolate's mechanism of action in a lysolecithin-induced demyelination model using organotypic culture of cerebellar slices. Etazolate treatment was able to i) enhance the release of sAPPα in the culture media of demyelinated slices, ii) protect myelinated axons from demyelination, iii) increase the number of mature oligodendrocytes, iv) promote the reappearance of the paired Caspr
+ adjacent to the nodes of Ranvier and v) increase the percentage of myelinated axons with short internodes, an indicator of remyelination. Etazolate failed to promote all the aforementioned effects in the presence of GI254023X, an α-secretase inhibitor. Moreover, the protective effects of etazolate in demyelinated slices were mimicked by sAPPα treatment in a dose-dependent manner. In conclusion, etazolate-induced sAPPα release protects myelinated axons from demyelination while also promoting remyelination. This work, thus, highlights the therapeutic potential of strategies that enhance sAPPα release in demyelinating disorders., (Copyright © 2017 Elsevier Inc. All rights reserved.)- Published
- 2018
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8. Corrigendum: Scavenger receptor collectin placenta 1 is a novel receptor involved in the uptake of myelin by phagocytes.
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Bogie JFJ, Mailleux J, Wouters E, Jorissen W, Grajchen E, Vanmol J, Wouters K, Hellings N, Horssen JV, Vanmierlo T, and Hendriks JJA
- Abstract
This corrects the article DOI: 10.1038/srep44794.
- Published
- 2017
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9. Low-Density Lipoprotein Receptor Deficiency Attenuates Neuroinflammation through the Induction of Apolipoprotein E.
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Mailleux J, Timmermans S, Nelissen K, Vanmol J, Vanmierlo T, van Horssen J, Bogie JFJ, and Hendriks JJA
- Abstract
Objective: We aimed to determine the role of the low-density lipoprotein receptor (LDLr) in neuroinflammation by inducing experimental autoimmune encephalomyelitis (EAE) in ldlr knock out mice., Methods: MOG
35-55 induced EAE in male and female ldlr-/- mice was assessed clinically and histopathologically. Expression of inflammatory mediators and apolipoprotein E (apoE) was investigated by qPCR. Changes in protein levels of apoE and tumor necrosis factor alpha (TNFα) were validated by western blot and ELISA, respectively., Results: Ldlr-/- -attenuated EAE disease severity in female, but not in male, EAE mice marked by a reduced proinflammatory cytokine production in the central nervous system of female ldlr-/- mice. Macrophages from female ldlr-/- mice showed a similar decrease in proinflammatory mediators, an impaired capacity to phagocytose myelin and enhanced secretion of the anti-inflammatory apoE. Interestingly, apoE/ldlr double knock out abrogated the beneficial effect of ldlr depletion in EAE., Conclusion: Collectively, we show that ldlr-/- reduces EAE disease severity in female but not in male EAE mice, and that this can be explained by increased levels of apoE in female ldlr-/- mice. Although the reason for the observed sexual dimorphism remains unclear, our findings show that LDLr and associated apoE levels are involved in neuroinflammatory processes.- Published
- 2017
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10. Scavenger receptor collectin placenta 1 is a novel receptor involved in the uptake of myelin by phagocytes.
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Bogie JF, Mailleux J, Wouters E, Jorissen W, Grajchen E, Vanmol J, Wouters K, Hellings N, van Horssen J, Vanmierlo T, and Hendriks JJ
- Subjects
- Animals, Cell Membrane metabolism, HEK293 Cells, Humans, Mice, Mice, Inbred C57BL, Multiple Sclerosis pathology, Myeloid Cells metabolism, RAW 264.7 Cells, Collectins metabolism, Myelin Sheath metabolism, Phagocytes metabolism, Receptors, Scavenger metabolism
- Abstract
Myelin-containing macrophages and microglia are the most abundant immune cells in active multiple sclerosis (MS) lesions. Our recent transcriptomic analysis demonstrated that collectin placenta 1 (CL-P1) is one of the most potently induced genes in macrophages after uptake of myelin. CL-P1 is a type II transmembrane protein with both a collagen-like and carbohydrate recognition domain, which plays a key role in host defense. In this study we sought to determine the dynamics of CL-P1 expression on myelin-containing phagocytes and define the role that it plays in MS lesion development. We show that myelin uptake increases the cell surface expression of CL-P1 by mouse and human macrophages, but not by primary mouse microglia in vitro. In active demyelinating MS lesions, CL-P1 immunoreactivity was localized to perivascular and parenchymal myelin-laden phagocytes. Finally, we demonstrate that CL-P1 is involved in myelin internalization as knockdown of CL-P1 markedly reduced myelin uptake. Collectively, our data indicate that CL-P1 is a novel receptor involved in myelin uptake by phagocytes and likely plays a role in MS lesion development.
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- 2017
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11. Plant sterols: Friend or foe in CNS disorders?
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Vanmierlo T, Bogie JF, Mailleux J, Vanmol J, Lütjohann D, Mulder M, and Hendriks JJ
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- Animals, Central Nervous System Diseases drug therapy, Central Nervous System Diseases pathology, Humans, Multiple Sclerosis drug therapy, Multiple Sclerosis metabolism, Phytosterols therapeutic use, Central Nervous System Diseases metabolism, Phytosterols metabolism
- Abstract
In mammals, the central nervous system (CNS) is the most cholesterol rich organ by weight. Cholesterol metabolism is tightly regulated in the CNS and all cholesterol available is synthesized in situ. Deficits in cholesterol homeostasis at the level of synthesis, transport, or catabolism result in severe disorders featured by neurological disability. Recent studies indicate that a disturbed cholesterol metabolism is involved in CNS disorders, such as Alzheimer's disease (AD), multiple sclerosis (MS), and amyotrophic lateral sclerosis (ALS). In contrast to circulating cholesterol, dietary plant sterols, can cross the blood-brain barrier and accumulate in the membranes of CNS cells. Plant sterols are well-known for their ability to lower circulating cholesterol levels. The finding that they gain access to the CNS has fueled research focusing on the physiological roles of plant sterols in the healthy and diseased CNS. To date, both beneficial and detrimental effects of plant sterols on CNS disorders are defined. In this review, we discuss recent findings regarding the impact of plant sterols on homeostatic and pathogenic processes in the CNS, and elaborate on the therapeutic potential of plant sterols in CNS disorders., (Copyright © 2015 Elsevier Ltd. All rights reserved.)
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- 2015
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12. Myelin alters the inflammatory phenotype of macrophages by activating PPARs.
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Bogie JF, Jorissen W, Mailleux J, Nijland PG, Zelcer N, Vanmierlo T, Van Horssen J, Stinissen P, Hellings N, and Hendriks JJ
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- Adult, Aged, Animals, Brain immunology, Brain pathology, Cell Proliferation physiology, Cells, Cultured, Encephalomyelitis, Autoimmune, Experimental immunology, Encephalomyelitis, Autoimmune, Experimental pathology, Female, Humans, Lysosomes metabolism, Male, Middle Aged, Multiple Sclerosis pathology, Nitric Oxide metabolism, Phosphatidylserines administration & dosage, Phosphatidylserines metabolism, Rats, Spleen immunology, T-Lymphocytes physiology, Macrophages immunology, Multiple Sclerosis immunology, Myelin Sheath physiology, PPAR delta metabolism, PPAR-beta metabolism
- Abstract
Background: Foamy macrophages, containing myelin degradation products, are abundantly found in active multiple sclerosis (MS) lesions. Recent studies have described an altered phenotype of macrophages after myelin internalization. However, mechanisms by which myelin affects the phenotype of macrophages and how this phenotype influences lesion progression remain unclear., Results: We demonstrate that myelin as well as phosphatidylserine (PS), a phospholipid found in myelin, reduce nitric oxide production by macrophages through activation of peroxisome proliferator-activated receptor β/δ (PPARβ/δ). Furthermore, uptake of PS by macrophages, after intravenous injection of PS-containing liposomes (PSLs), suppresses the production of inflammatory mediators and ameliorates experimental autoimmune encephalomyelitis (EAE), an animal model of MS. The protective effect of PSLs in EAE animals is associated with a reduced immune cell infiltration into the central nervous system and decreased splenic cognate antigen specific proliferation. Interestingly, PPARβ/δ is activated in foamy macrophages in active MS lesions, indicating that myelin also activates PPARβ/δ in macrophages in the human brain., Conclusion: Our data show that myelin modulates the phenotype of macrophages by PPAR activation, which may subsequently dampen MS lesion progression. Moreover, our results suggest that myelin-derived PS mediates PPARβ/δ activation in macrophages after myelin uptake. The immunoregulatory impact of naturally-occurring myelin lipids may hold promise for future MS therapeutics.
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- 2013
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13. [Pulmonary complications of malaria. Apropos of 2 cases].
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Lessire H, Coyette Y, Lambert M, Mailleux JP, Coche E, and Reynaert M
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- Adult, Female, Humans, Male, Middle Aged, Plasmodium falciparum, Pulmonary Edema therapy, Respiratory Distress Syndrome therapy, Malaria complications, Pulmonary Edema etiology, Respiratory Distress Syndrome etiology
- Published
- 1984
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