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Article ; Online: Systemic sterile induced-co-expression of IL-12 and IL-18 drive IFN-γ-dependent activation of microglia and recruitment of MHC-II-expressing inflammatory monocytes into the brain.

Gaviglio, Emilia A / Peralta Ramos, Javier M / Arroyo, Daniela S / Bussi, Claudio / Iribarren, Pablo / Rodriguez-Galan, Maria C

International immunopharmacology

2022 Volume 105, Page(s) 108546

Abstract: The development of neuroinflammation, as well as the progression of several neurodegenerative diseases, has been associated with the activation and mobilization of the peripheral immune system due to systemic inflammation. However, the mechanism by which ...

Abstract	The development of neuroinflammation, as well as the progression of several neurodegenerative diseases, has been associated with the activation and mobilization of the peripheral immune system due to systemic inflammation. However, the mechanism by which this occurs remains unclear. Here, we addressed the effect of systemic sterile induced-co-expression of IL-12 and IL-18, in the establishment of a novel cytokine-mediated model of neuroinflammation. Following peripheral hydrodynamic shear of IL-12 plus IL-18 cDNAs in C57BL/6 mice, we induced systemic and persistent level of IL-12, which in turn promoted the elevation of circulating pro-inflammatory cytokines TNF-α and IFN-γ, accompanied with splenomegaly. Moreover, even though we identified an increased gene expression of both TNF-α and IFN-γ in the brain, we observed that only IFN-γ, but not TNF-α signaling through its type I receptor, was required to induce both the trafficking of leukocytes from the periphery toward the brain and upregulate MHC-II in microglia and inflammatory monocytes. Therefore, only TNF-α was shown to be dispensable, revealing an IFN-γ-dependent activation of microglia and recruitment of leukocytes, particularly of highly activated inflammatory monocytes. Taken together, our results argue for a systemic cytokine-mediated establishment and development of neuroinflammation, having identified IFN-γ as a potential target for immunomodulation.
MeSH term(s)	Animals ; Brain/metabolism ; Cytokines/metabolism ; Interferon-gamma/metabolism ; Interleukin-12/metabolism ; Interleukin-18/metabolism ; Mice ; Mice, Inbred C57BL ; Microglia/metabolism ; Monocytes/metabolism ; Tumor Necrosis Factor-alpha/metabolism
Chemical Substances	Cytokines ; Interleukin-18 ; Tumor Necrosis Factor-alpha ; Interleukin-12 (187348-17-0) ; Interferon-gamma (82115-62-6)
Language	English
Publishing date	2022-01-21
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2043785-7
ISSN	1878-1705 ; 1567-5769
ISSN (online)	1878-1705
ISSN	1567-5769
DOI	10.1016/j.intimp.2022.108546
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Article: Increased Expression of Autophagy Protein LC3 in Two Patients With Progressing Chronic Lymphocytic Leukemia.

Arroyo, Daniela S / Rodriguez, Cecilia M / Bussi, Claudio / Manzone-Rodriguez, Clarisa / Sastre, Darío / Heller, Viviana / Stanganelli, Carmen / Slavutsky, Irma / Iribarren, Pablo

Frontiers in endocrinology

2020 Volume 11, Page(s) 321

Abstract: Chronic lymphocytic leukemia (CLL) is the most common type of adult leukemia in the western hemisphere. It is characterized by a clonal proliferation of a population of CD5+ B lymphocytes that accumulate in the secondary lymphoid tissues, bone marrow, ... ...

Abstract	Chronic lymphocytic leukemia (CLL) is the most common type of adult leukemia in the western hemisphere. It is characterized by a clonal proliferation of a population of CD5+ B lymphocytes that accumulate in the secondary lymphoid tissues, bone marrow, and blood. Some CLL patients remain free of symptoms for decades, whereas others rapidly become symptomatic or develop high-risk disease. Studying autophagy, which may modulate key protein expression and cell survival, may be important to the search for novel prognostic factors and molecules. Here, we applied flow cytometry technology to simultaneously detect autophagy protein LC3B with classical phenotypical markers used for the identification of tumoral CLL B cell clones. We found that two patients with progressing CLL showed increased expression of the autophagy protein LC3B, in addition to positive expression of CD38 and ZAP70 and unmutated status of IGHV. Our data suggest that activation of autophagy flux may correlate with CLL progression even before Ibrutinib treatment.
MeSH term(s)	Adult ; Autophagy ; Disease Progression ; Female ; Humans ; Leukemia, Lymphocytic, Chronic, B-Cell/metabolism ; Leukemia, Lymphocytic, Chronic, B-Cell/pathology ; Male ; Microtubule-Associated Proteins/metabolism ; Middle Aged ; Mutation ; Prognosis
Chemical Substances	MAP1LC3A protein, human ; Microtubule-Associated Proteins
Language	English
Publishing date	2020-07-22
Publishing country	Switzerland
Document type	Case Reports ; Research Support, Non-U.S. Gov't
ZDB-ID	2592084-4
ISSN	1664-2392
ISSN	1664-2392
DOI	10.3389/fendo.2020.00321
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Article: Phosphatidyl-Inositol-3 Kinase Inhibitors Regulate Peptidoglycan-Induced Myeloid Leukocyte Recruitment, Inflammation, and Neurotoxicity in Mouse Brain.

Arroyo, Daniela S / Gaviglio, Emilia A / Peralta Ramos, Javier M / Bussi, Claudio / Avalos, Maria P / Cancela, Liliana M / Iribarren, Pablo

Frontiers in immunology

2018 Volume 9, Page(s) 770

Abstract: Acute brain injury leads to the recruitment and activation of immune cells including resident microglia and infiltrating peripheral myeloid cells (MC), which contribute to the inflammatory response involved in neuronal damage. We previously reported that ...

Abstract	Acute brain injury leads to the recruitment and activation of immune cells including resident microglia and infiltrating peripheral myeloid cells (MC), which contribute to the inflammatory response involved in neuronal damage. We previously reported that TLR2 stimulation by peptidoglycan (PGN) from
MeSH term(s)	Adenine/analogs & derivatives ; Adenine/pharmacology ; Animals ; Autophagy/drug effects ; Brain/drug effects ; Brain/immunology ; Chemotaxis, Leukocyte/drug effects ; Chemotaxis, Leukocyte/immunology ; Enzyme Inhibitors/pharmacology ; Inflammation/enzymology ; Inflammation/immunology ; Male ; Mice ; Mice, Inbred C57BL ; Microglia/drug effects ; Microglia/immunology ; Microglia/metabolism ; Peptidoglycan/toxicity ; Phosphatidylinositol 3-Kinases/antagonists & inhibitors
Chemical Substances	Enzyme Inhibitors ; Peptidoglycan ; 3-methyladenine (5142-23-4) ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Adenine (JAC85A2161)
Language	English
Publishing date	2018-04-17
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2018.00770
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Article ; Online: Effects of rapamycin in combination with fludarabine on primary chronic lymphocytic leukemia cells.

Rodriguez, Cecilia M / Bussi, Claudio / Arroyo, Daniela S / Sastre, Dario / Heller, Viviana / Stanganelli, Carmen / Slavutsky, Irma / Iribarren, Pablo

Leukemia & lymphoma

2018 Volume 60, Issue 5, Page(s) 1299–1303

MeSH term(s)	Antineoplastic Combined Chemotherapy Protocols/adverse effects ; Antineoplastic Combined Chemotherapy Protocols/therapeutic use ; Biomarkers ; Biomarkers, Tumor ; Disease Susceptibility ; Female ; Flow Cytometry ; Gene Expression ; Humans ; Leukemia, Lymphocytic, Chronic, B-Cell/diagnosis ; Leukemia, Lymphocytic, Chronic, B-Cell/drug therapy ; Leukemia, Lymphocytic, Chronic, B-Cell/etiology ; Leukemia, Lymphocytic, Chronic, B-Cell/mortality ; Male ; Mutation ; Sirolimus/administration & dosage ; Treatment Outcome ; Vidarabine/administration & dosage ; Vidarabine/analogs & derivatives
Chemical Substances	Biomarkers ; Biomarkers, Tumor ; Vidarabine (FA2DM6879K) ; fludarabine (P2K93U8740) ; Sirolimus (W36ZG6FT64)
Language	English
Publishing date	2018-11-08
Publishing country	United States
Document type	Letter ; Research Support, Non-U.S. Gov't
ZDB-ID	1042374-6
ISSN	1029-2403 ; 1042-8194
ISSN (online)	1029-2403
ISSN	1042-8194
DOI	10.1080/10428194.2018.1529309
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Zs.A 2997: Show issues

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Article ; Online: Autophagy down regulates pro-inflammatory mediators in BV2 microglial cells and rescues both LPS and alpha-synuclein induced neuronal cell death.

Bussi, Claudio / Peralta Ramos, Javier Maria / Arroyo, Daniela S / Gaviglio, Emilia A / Gallea, Jose Ignacio / Wang, Ji Ming / Celej, Maria Soledad / Iribarren, Pablo

Scientific reports

2017 Volume 7, Page(s) 43153

Abstract: Autophagy is a fundamental cellular homeostatic mechanism, whereby cells autodigest parts of their cytoplasm for removal or turnover. Neurodegenerative disorders are associated with autophagy dysregulation, and drugs modulating autophagy have been ... ...

Abstract	Autophagy is a fundamental cellular homeostatic mechanism, whereby cells autodigest parts of their cytoplasm for removal or turnover. Neurodegenerative disorders are associated with autophagy dysregulation, and drugs modulating autophagy have been successful in several animal models. Microglial cells are phagocytes in the central nervous system (CNS) that become activated in pathological conditions and determine the fate of other neural cells. Here, we studied the effects of autophagy on the production of pro-inflammatory molecules in microglial cells and their effects on neuronal cells. We observed that both trehalose and rapamycin activate autophagy in BV2 microglial cells and down-regulate the production of pro-inflammatory cytokines and nitric oxide (NO), in response to LPS and alpha-synuclein. Autophagy also modulated the phosphorylation of p38 and ERK1/2 MAPKs in BV2 cells, which was required for NO production. These actions of autophagy modified the impact of microglial activation on neuronal cells, leading to suppression of neurotoxicity. Our results demonstrate a novel role for autophagy in the regulation of microglial cell activation and pro-inflammatory molecule secretion, which may be important for the control of inflammatory responses in the CNS and neurotoxicity.
MeSH term(s)	Animals ; Autophagy ; Cell Death/drug effects ; Cell Line ; Cytokines/metabolism ; Lipopolysaccharides/toxicity ; Mice ; Neuroglia/physiology ; Nitric Oxide/metabolism ; Signal Transduction ; alpha-Synuclein/toxicity
Chemical Substances	Cytokines ; Lipopolysaccharides ; alpha-Synuclein ; Nitric Oxide (31C4KY9ESH)
Language	English
Publishing date	2017-03-03
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/srep43153
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Article ; Online: Alpha-synuclein fibrils recruit TBK1 and OPTN to lysosomal damage sites and induce autophagy in microglial cells.

Bussi, Claudio / Peralta Ramos, Javier M / Arroyo, Daniela S / Gallea, Jose I / Ronchi, Paolo / Kolovou, Androniki / Wang, Ji M / Florey, Oliver / Celej, Maria S / Schwab, Yannick / Ktistakis, Nicholas T / Iribarren, Pablo

Journal of cell science

2018 Volume 131, Issue 23

Abstract: Autophagic dysfunction and protein aggregation have been linked to several neurodegenerative disorders, but the exact mechanisms and causal connections are not clear and most previous work was done in neurons and not in microglial cells. Here, we report ... ...

Abstract	Autophagic dysfunction and protein aggregation have been linked to several neurodegenerative disorders, but the exact mechanisms and causal connections are not clear and most previous work was done in neurons and not in microglial cells. Here, we report that exogenous fibrillary, but not monomeric, alpha-synuclein (AS, also known as SNCA) induces autophagy in microglial cells. We extensively studied the dynamics of this response using both live-cell imaging and correlative light-electron microscopy (CLEM), and found that it correlates with lysosomal damage and is characterised by the recruitment of the selective autophagy-associated proteins TANK-binding kinase 1 (TBK1) and optineurin (OPTN) to ubiquitylated lysosomes. In addition, we observed that LC3 (MAP1LC3B) recruitment to damaged lysosomes was dependent on TBK1 activity. In these fibrillar AS-treated cells, autophagy inhibition impairs mitochondrial function and leads to microglial cell death. Our results suggest that microglial autophagy is induced in response to lysosomal damage caused by persistent accumulation of AS fibrils. Importantly, triggering of the autophagic response appears to be an attempt at lysosomal quality control and not for engulfment of fibrillar AS.This article has an associated First Person interview with the first author of the paper.
MeSH term(s)	Autophagy ; Cell Cycle Proteins ; Humans ; Lysosomes/metabolism ; Membrane Transport Proteins ; Microglia/metabolism ; Protein Serine-Threonine Kinases/genetics ; Protein Serine-Threonine Kinases/metabolism ; Signal Transduction ; Transcription Factor TFIIIA/genetics ; Transcription Factor TFIIIA/metabolism ; alpha-Synuclein/metabolism
Chemical Substances	Cell Cycle Proteins ; Membrane Transport Proteins ; OPTN protein, human ; Transcription Factor TFIIIA ; alpha-Synuclein ; Protein Serine-Threonine Kinases (EC 2.7.11.1) ; TBK1 protein, human (EC 2.7.11.1)
Language	English
Publishing date	2018-11-30
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2993-2
ISSN	1477-9137 ; 0021-9533
ISSN (online)	1477-9137
ISSN	0021-9533
DOI	10.1242/jcs.226241
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Zs.A 1200: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 14: Show issues

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Article ; Online: Toll-like receptors are key players in neurodegeneration.

Arroyo, Daniela S / Soria, Javier A / Gaviglio, Emilia A / Rodriguez-Galan, Maria C / Iribarren, Pablo

International immunopharmacology

2011 Volume 11, Issue 10, Page(s) 1415–1421

Abstract: The activation of innate immune response is initiated by engagement of pattern-recognition receptors (PPRs), such as Toll-like receptors (TLRs). These receptors are expressed in peripheral leukocytes and in many cell types in the central nervous system ( ... ...

Abstract	The activation of innate immune response is initiated by engagement of pattern-recognition receptors (PPRs), such as Toll-like receptors (TLRs). These receptors are expressed in peripheral leukocytes and in many cell types in the central nervous system (CNS). The expression of TLRs in CNS was mainly studied in astrocytes and microglial cells. However, new evidence indicates that these receptors may play an important role in neuronal homeostasis. The expression of TLRs in the CNS is variable and can be modulated by multiple factors, including pro-inflammatory molecules, which are elevated in neurodegenerative diseases and can increase the expression of TLRs in CNS cells. Moreover, activation of TLRs induces the release of pro-inflammatory cytokines. Therefore, TLRs have been shown to play a role in several aspects of neurodegenerative diseases. Here we will discuss results reported in the recent literature concerning the participation of TLRs in neurodegenerative diseases.
MeSH term(s)	Animals ; Astrocytes/immunology ; Cell Survival/immunology ; Cellular Microenvironment/immunology ; Central Nervous System/immunology ; Central Nervous System/metabolism ; Central Nervous System/pathology ; Cytokines/immunology ; Cytokines/metabolism ; Gene Expression Regulation/immunology ; Humans ; Inflammation ; Inflammation Mediators/immunology ; Inflammation Mediators/metabolism ; Microglia/immunology ; Molecular Targeted Therapy ; Neurodegenerative Diseases/drug therapy ; Neurodegenerative Diseases/immunology ; Neurodegenerative Diseases/physiopathology ; Neurons/physiology ; Toll-Like Receptors/agonists ; Toll-Like Receptors/antagonists & inhibitors ; Toll-Like Receptors/immunology
Chemical Substances	Cytokines ; Inflammation Mediators ; Toll-Like Receptors
Language	English
Publishing date	2011-05-25
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2043785-7
ISSN	1878-1705 ; 1567-5769
ISSN (online)	1878-1705
ISSN	1567-5769
DOI	10.1016/j.intimp.2011.05.006
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Article ; Online: Autophagy in inflammation, infection, neurodegeneration and cancer.

Arroyo, Daniela S / Gaviglio, Emilia A / Peralta Ramos, Javier M / Bussi, Claudio / Rodriguez-Galan, Maria C / Iribarren, Pablo

International immunopharmacology

2013 Volume 18, Issue 1, Page(s) 55–65

Abstract: In its classical form, autophagy is an essential, homeostatic process by which cytoplasmic components are degraded in a double-membrane-bound autophagosome in response to starvation. Paradoxically, although autophagy is primarily a protective process for ...

Abstract	In its classical form, autophagy is an essential, homeostatic process by which cytoplasmic components are degraded in a double-membrane-bound autophagosome in response to starvation. Paradoxically, although autophagy is primarily a protective process for the cell, it can also play a role in cell death. The roles of autophagy bridge both the innate and adaptive immune systems and autophagic dysfunction is associated with inflammation, infection, neurodegeneration and cancer. In this review, we discuss the contribution of autophagy to inflammatory, infectious and neurodegenerative diseases, as well as cancer.
MeSH term(s)	Adaptive Immunity ; Animals ; Autophagy ; Cellular Structures/metabolism ; Homeostasis ; Humans ; Immunity, Innate ; Infections/physiopathology ; Inflammation/physiopathology ; Neoplasms/physiopathology ; Neurodegenerative Diseases/physiopathology ; Phagosomes/metabolism
Language	English
Publishing date	2013-11-19
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2043785-7
ISSN	1878-1705 ; 1567-5769
ISSN (online)	1878-1705
ISSN	1567-5769
DOI	10.1016/j.intimp.2013.11.001
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Article ; Online: Interleukin 4 induces the apoptosis of mouse microglial cells by a caspase-dependent mechanism.

Soria, Javier A / Arroyo, Daniela S / Gaviglio, Emilia A / Rodriguez-Galan, Maria C / Wang, Ji Ming / Iribarren, Pablo

Neurobiology of disease

2011 Volume 43, Issue 3, Page(s) 616–624

Abstract: Microglial cells are resident macrophages in the central nervous system (CNS) and become activated in many pathological conditions. Activation of microglial cells results in reactive microgliosis, manifested by an increase in cell number in the affected ... ...

Abstract	Microglial cells are resident macrophages in the central nervous system (CNS) and become activated in many pathological conditions. Activation of microglial cells results in reactive microgliosis, manifested by an increase in cell number in the affected CNS regions. The control of microgliosis may be important to prevent pathological damage to the brain. The type 2 cytokine IL-4 has been reported to be protective in brain inflammation. However, its effect on microglial cell survival was not well understood. In this study, we report a dual effect of IL-4 on the survival of mouse microglial cells. In a 6h short term culture, IL-4 reduced the death of microglial cells induced by staurosporine. In contrast, in long term treatment (more than 48h), IL-4 increased the apoptotic death of both primary mouse microglial cells and a microglial cell line N9. Mechanistic studies revealed that, in microglial cells, IL-4 increased the levels of cleaved caspase 3 and PARP, which is down-stream of activated caspase 3. In addition, IL-4 down regulated the autophagy and the antiapoptotic protein Bcl-xL in microglial cells. On the other hand, the pre-incubation of microglial cells with IL-4 for 24h, attenuated the cell death induced by the neurotoxic peptide amyloid beta 1-42 (Aβ42). Our observations demonstrate a novel function of IL-4 in regulating the survival of microglial cells, which may have important significance in reduction of undesired inflammatory responses in the CNS.
MeSH term(s)	Amyloid beta-Peptides/toxicity ; Animals ; Apoptosis/immunology ; Caspase 3/physiology ; Caspase Inhibitors ; Cell Survival/immunology ; Cells, Cultured ; Inflammation Mediators/antagonists & inhibitors ; Inflammation Mediators/physiology ; Interleukin-4/physiology ; Mice ; Mice, Inbred C57BL ; Microglia/enzymology ; Microglia/immunology ; Microglia/pathology ; Peptide Fragments/toxicity ; Poly (ADP-Ribose) Polymerase-1 ; Poly(ADP-ribose) Polymerases/biosynthesis ; Poly(ADP-ribose) Polymerases/metabolism ; Staurosporine/pharmacology
Chemical Substances	Amyloid beta-Peptides ; Caspase Inhibitors ; Inflammation Mediators ; Peptide Fragments ; amyloid beta-protein (1-42) ; Interleukin-4 (207137-56-2) ; Parp1 protein, mouse (EC 2.4.2.30) ; Poly (ADP-Ribose) Polymerase-1 (EC 2.4.2.30) ; Poly(ADP-ribose) Polymerases (EC 2.4.2.30) ; Casp3 protein, mouse (EC 3.4.22.-) ; Caspase 3 (EC 3.4.22.-) ; Staurosporine (H88EPA0A3N)
Language	English
Publishing date	2011-05-23
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1211786-9
ISSN	1095-953X ; 0969-9961
ISSN (online)	1095-953X
ISSN	0969-9961
DOI	10.1016/j.nbd.2011.05.010
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Article ; Online: Toll-like receptor 2 ligands promote microglial cell death by inducing autophagy.

Arroyo, Daniela S / Soria, Javier A / Gaviglio, Emilia A / Garcia-Keller, Constanza / Cancela, Liliana M / Rodriguez-Galan, Maria C / Wang, Ji Ming / Iribarren, Pablo

FASEB journal : official publication of the Federation of American Societies for Experimental Biology

2012 Volume 27, Issue 1, Page(s) 299–312

Abstract: Microglial cells are phagocytes in the central nervous system (CNS) and become activated in pathological conditions, resulting in microgliosis, manifested by increased cell numbers and inflammation in the affected regions. Thus, controlling microgliosis ... ...

Abstract	Microglial cells are phagocytes in the central nervous system (CNS) and become activated in pathological conditions, resulting in microgliosis, manifested by increased cell numbers and inflammation in the affected regions. Thus, controlling microgliosis is important to prevent pathological damage to the brain. Here, we evaluated the contribution of Toll-like receptor 2 (TLR2) to microglial survival. We observed that activation of microglial cells with peptidoglycan (PGN) from Staphylococcus aureus and other TLR2 ligands results in cell activation followed by the induction of autophagy and autophagy-dependent cell death. In C57BL/6J mice, intracerebral injection of PGN increased the autophagy of microglial cells and reduced the microglial/macrophage cell number in brain parenchyma. Our results demonstrate a novel role of TLRs in the regulation of microglial cell activation and survival, which are important for the control of microgliosis and associated inflammatory responses in the CNS.
MeSH term(s)	Animals ; Autophagy ; Blotting, Western ; Cell Death/physiology ; Flow Cytometry ; Ligands ; Male ; Mice ; Mice, Inbred C57BL ; Microglia/cytology ; Microscopy, Confocal ; Microscopy, Electron, Transmission ; Polysaccharides/metabolism ; Polysaccharides/physiology ; Toll-Like Receptor 2/metabolism
Chemical Substances	Ligands ; Polysaccharides ; Toll-Like Receptor 2
Language	English
Publishing date	2012-10-16
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	639186-2
ISSN	1530-6860 ; 0892-6638
ISSN (online)	1530-6860
ISSN	0892-6638
DOI	10.1096/fj.12-214312
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