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Article: Editorial: Sphingolipids in Infection Control.

Seibel, Jürgen / Schneider-Schaulies, Sibylle / Kleuser, Burkhard

Frontiers in cell and developmental biology

2021 Volume 9, Page(s) 697290

Language	English
Publishing date	2021-06-21
Publishing country	Switzerland
Document type	Editorial
ZDB-ID	2737824-X
ISSN	2296-634X
ISSN	2296-634X
DOI	10.3389/fcell.2021.697290
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Article ; Online: CD4+ Foxp3+ regulatory T cell-mediated immunomodulation by anti-depressants inhibiting acid sphingomyelinase.

Schneider-Schaulies, Jürgen / Beyersdorf, Niklas

Biological chemistry

2018 Volume 399, Issue 10, Page(s) 1175–1182

Abstract: Acid sphingomyelinase (ASM) is the rate-limiting enzyme cleaving sphingomyelin into ceramide and phosphorylcholin. CD4+ Foxp3+ regulatory T (Treg) cells depend on CD28 signaling for their survival and function, a receptor that activates the ASM. Both, ... ...

Abstract	Acid sphingomyelinase (ASM) is the rate-limiting enzyme cleaving sphingomyelin into ceramide and phosphorylcholin. CD4+ Foxp3+ regulatory T (Treg) cells depend on CD28 signaling for their survival and function, a receptor that activates the ASM. Both, basal and CD28-induced ASM activities are higher in Treg cells than in conventional CD4+ T (Tconv) cells. In ASM-deficient (Smpd1-/-) as compared to wt mice, membranes of T cells contain 7-10-fold more sphingomyelin and two- to three-fold more ceramide, and are in a state of higher order than membranes of T cells from wt mice, which may facilitate their activation. Indeed, the frequency of Treg cells among CD4+ T cells in ASM-deficient mice and their suppressive activity in vitro are increased. Moreover, in vitro stimulation of ASM-deficient T cells in the presence of TGF-β and IL-2 leads to higher numbers of induced Treg cells. Pharmacological inhibition of the ASM with a clinically used tricyclic antidepressant such as amitriptyline in mice or in tissue culture of murine or human T cells induces higher frequencies of Treg cells among CD4+ T cells within a few days. This fast alteration of the balance between T cell populations in vitro is due to the elevated cell death of Tconv cells and protection of the CD25high Treg cells by IL-2. Together, these findings suggest that ASM-inhibiting antidepressants, including a fraction of the serotonin re-uptake inhibitors (SSRIs), are moderately immunosuppressive and should be considered for the therapy of inflammatory and autoimmune disorders.
MeSH term(s)	Amitriptyline/pharmacology ; Animals ; Antidepressive Agents/pharmacology ; Autoimmune Diseases/therapy ; Forkhead Transcription Factors/metabolism ; Humans ; Immunomodulation/drug effects ; Inflammation/therapy ; Mice ; Sphingomyelin Phosphodiesterase/antagonists & inhibitors ; Sphingomyelin Phosphodiesterase/deficiency ; Sphingomyelin Phosphodiesterase/metabolism ; T-Lymphocytes, Regulatory/immunology ; T-Lymphocytes, Regulatory/metabolism
Chemical Substances	Antidepressive Agents ; FOXP3 protein, human ; Forkhead Transcription Factors ; Foxp3 protein, mouse ; Amitriptyline (1806D8D52K) ; Sphingomyelin Phosphodiesterase (EC 3.1.4.12)
Language	English
Publishing date	2018-04-27
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1334659-3
ISSN	1437-4315 ; 1431-6730 ; 1432-0355
ISSN (online)	1437-4315
ISSN	1431-6730 ; 1432-0355
DOI	10.1515/hsz-2018-0159
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Article: The Sphingolipid Inhibitors Ceranib-2 and SKI-II Reduce Measles Virus Replication in Primary Human Lymphocytes: Effects on mTORC1 Downstream Signaling.

Chithelen, Janice / Franke, Hannah / Länder, Nora / Grafen, Anika / Schneider-Schaulies, Jürgen

Frontiers in physiology

2022 Volume 13, Page(s) 856143

Abstract: The bioactive sphingolipids ceramide and sphingosine-1-phosphate (S1P) are involved in the regulation of cell homeostasis and activity ranging from apoptosis to proliferation. We recently described that the two compounds ceranib-2 (inhibiting acid ... ...

Abstract	The bioactive sphingolipids ceramide and sphingosine-1-phosphate (S1P) are involved in the regulation of cell homeostasis and activity ranging from apoptosis to proliferation. We recently described that the two compounds ceranib-2 (inhibiting acid ceramidase) and SKI-II [inhibiting the sphingosine kinases 1 and - 2 (SphK1/2)] reduce mTORC1 activity and measles virus (MV) replication in human primary peripheral blood lymphocytes (PBL) by about one log step. We now further investigated whether mTORC1 downstream signaling and viral protein expression may be affected by ceranib-2 and/or SKI-II. Western blot analyses showed that in uninfected cells the phosphorylation of the eukaryotic initiation factor 4E (eIF4E) was reduced by both inhibitors. Interestingly, MV infection led to an increase of rpS6 protein levels and phosphorylation of eIF4E. Treatment with both inhibitors reduced the rpS6 protein expression, and in addition, SKI-II reduced rpS6 phosphorylation. The phosphorylation of eIF4E was slightly reduced by both inhibitors. In addition, SKI-II led to reduced levels of IKK in MV-infected cells. Both inhibitors reduced the expression of viral proteins and the titers of newly synthesized MV by approximately one log step. As expected, SKI-II and rapamycin reduced also the virally encoded GFP expression; however, ceranib-2 astonishingly led to increased levels of GFP fluorescence. Our findings suggest that the inhibitors ceranib-2 and SKI-II act
Language	English
Publishing date	2022-03-17
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2564217-0
ISSN	1664-042X
ISSN	1664-042X
DOI	10.3389/fphys.2022.856143
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Article ; Online: Sphingolipids in viral infection.

Schneider-Schaulies, Jürgen / Schneider-Schaulies, Sibylle

Biological chemistry

2015 Volume 396, Issue 6-7, Page(s) 585–595

Abstract: Viruses exploit membranes and their components such as sphingolipids in all steps of their life cycle including attachment and membrane fusion, intracellular transport, replication, protein sorting and budding. Examples for sphingolipid-dependent virus ... ...

Abstract	Viruses exploit membranes and their components such as sphingolipids in all steps of their life cycle including attachment and membrane fusion, intracellular transport, replication, protein sorting and budding. Examples for sphingolipid-dependent virus entry are found for: human immunodeficiency virus (HIV), which besides its protein receptors also interacts with glycosphingolipids (GSLs); rhinovirus, which promotes the formation of ceramide-enriched platforms and endocytosis; or measles virus (MV), which induces the surface expression of its own receptor CD150 via activation of sphingomyelinases (SMases). While SMase activation was implicated in Ebola virus (EBOV) attachment, the virus utilizes the cholesterol transporter Niemann-Pick C protein 1 (NPC1) as 'intracellular' entry receptor after uptake into endosomes. Differential activities of SMases also affect the intracellular milieu required for virus replication. Sindbis virus (SINV), for example, replicates better in cells lacking acid SMase (ASMase). Defined lipid compositions of viral assembly and budding sites influence virus release and infectivity, as found for hepatitis C virus (HCV) or HIV. And finally, viruses manipulate cellular signaling and the sphingolipid metabolism to their advantage, as for example influenza A virus (IAV), which activates sphingosine kinase 1 and the transcription factor NF-κB.
MeSH term(s)	Cell Line ; Ceramides/metabolism ; Humans ; Phosphotransferases (Alcohol Group Acceptor)/metabolism ; Sphingolipids/metabolism ; Sphingomyelin Phosphodiesterase/metabolism ; Virus Internalization ; Virus Physiological Phenomena
Chemical Substances	Ceramides ; Sphingolipids ; Phosphotransferases (Alcohol Group Acceptor) (EC 2.7.1.-) ; sphingosine kinase (EC 2.7.1.-) ; Sphingomyelin Phosphodiesterase (EC 3.1.4.12)
Language	English
Publishing date	2015-06
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1334659-3
ISSN	1437-4315 ; 1431-6730 ; 1432-0355
ISSN (online)	1437-4315
ISSN	1431-6730 ; 1432-0355
DOI	10.1515/hsz-2014-0273
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Article ; Online: KDELR2 Competes with Measles Virus Envelope Proteins for Cellular Chaperones Reducing Their Chaperone-Mediated Cell Surface Transport.

Tiwarekar, Vishakha / Fehrholz, Markus / Schneider-Schaulies, Jürgen

Viruses

2019 Volume 11, Issue 1

Abstract: Recently, we found that the cytidine deaminase APOBEC3G (A3G) inhibits measles (MV) replication. Using a microarray, we identified differential regulation of several host genes upon ectopic expression of A3G. One of the up-regulated genes, the ... ...

Abstract	Recently, we found that the cytidine deaminase APOBEC3G (A3G) inhibits measles (MV) replication. Using a microarray, we identified differential regulation of several host genes upon ectopic expression of A3G. One of the up-regulated genes, the endoplasmic reticulum (ER) protein retention receptor KDELR2, reduced MV replication ~5 fold when it was over-expressed individually in Vero and CEM-SS T cells. Silencing of KDELR2 in A3G-expressing Vero cells abrogated the antiviral activity induced by A3G, confirming its role as an A3G-regulated antiviral host factor. Recognition of the KDEL (Lys-Asp-Glu-Leu) motif by KDEL receptors initiates the retrograde transport of soluble proteins that have escaped the ER and play an important role in ER quality control. Although KDELR2 over-expression reduced MV titers in cell cultures, we observed no interaction between KDELR2 and the MV hemagglutinin (H) protein. Instead, KDELR2 retained chaperones in the ER, which are required for the correct folding and transport of the MV envelope glycoproteins H and fusion protein (F) to the cell surface. Our data indicate that KDELR2 competes with MV envelope proteins for binding to calnexin and GRP78/Bip, and that this interaction limits the availability of the chaperones for MV proteins, causing the reduction of virus spread and titers.
MeSH term(s)	Animals ; Calnexin/metabolism ; Chlorocebus aethiops ; Gene Expression Regulation ; Gene Silencing ; HEK293 Cells ; Heat-Shock Proteins/genetics ; Heat-Shock Proteins/metabolism ; Hemagglutinins, Viral/genetics ; Hemagglutinins, Viral/metabolism ; Host Microbial Interactions ; Humans ; Measles virus/genetics ; Measles virus/physiology ; Vero Cells ; Vesicular Transport Proteins/genetics ; Vesicular Transport Proteins/metabolism ; Viral Fusion Proteins/genetics ; Viral Fusion Proteins/metabolism ; Viral Load
Chemical Substances	Heat-Shock Proteins ; Hemagglutinins, Viral ; Vesicular Transport Proteins ; Viral Fusion Proteins ; hemagglutinin protein G, measles virus ; Calnexin (139873-08-8) ; KDELR2 protein, human (147097-18-5) ; molecular chaperone GRP78 (YCYIS6GADR)
Keywords	covid19
Language	English
Publishing date	2019-01-04
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2516098-9
ISSN	1999-4915 ; 1999-4915
ISSN (online)	1999-4915
ISSN	1999-4915
DOI	10.3390/v11010027
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Article: The Manifold Roles of Sphingolipids in Viral Infections.

Avota, Elita / Bodem, Jochen / Chithelen, Janice / Mandasari, Putri / Beyersdorf, Niklas / Schneider-Schaulies, Jürgen

Frontiers in physiology

2021 Volume 12, Page(s) 715527

Abstract: Sphingolipids are essential components of eukaryotic cells. In this review, we want to exemplarily illustrate what is known about the interactions of sphingolipids with various viruses at different steps of their replication cycles. This includes ... ...

Abstract	Sphingolipids are essential components of eukaryotic cells. In this review, we want to exemplarily illustrate what is known about the interactions of sphingolipids with various viruses at different steps of their replication cycles. This includes structural interactions during entry at the plasma membrane or endosomal membranes, early interactions leading to sphingolipid-mediated signal transduction, interactions with internal membranes and lipids during replication, and interactions during virus assembly and budding. Targeted interventions in sphingolipid metabolism - as far as they can be tolerated by cells and organisms - may open novel possibilities to support antiviral therapies. Human immunodeficiency virus type 1 (HIV-1) infections have intensively been studied, but for other viral infections, such as influenza A virus (IAV), measles virus (MV), hepatitis C virus (HCV), dengue virus, Ebola virus, and severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2), investigations are still in their beginnings. As many inhibitors of sphingolipid metabolism are already in clinical use against other diseases, repurposing studies for applications in some viral infections appear to be a promising approach.
Language	English
Publishing date	2021-09-29
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2564217-0
ISSN	1664-042X
ISSN	1664-042X
DOI	10.3389/fphys.2021.715527
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Article: Viral infections and sphingolipids.

Schneider-Schaulies, Jürgen / Schneider-Schaulies, Sibylle

Handbook of experimental pharmacology

2013 , Issue 216, Page(s) 321–340

Abstract: Besides their essential role in the immune system, sphingolipids and their metabolites are potential key regulators in the life cycle of obligatory intracellular pathogens such as viruses. They are involved in lateral and vertical segregation of ... ...

Abstract	Besides their essential role in the immune system, sphingolipids and their metabolites are potential key regulators in the life cycle of obligatory intracellular pathogens such as viruses. They are involved in lateral and vertical segregation of receptors required for attachment, membrane fusion and endocytosis, as well as in the intracellular replication, assembly and release of viruses. Glycosphingolipids may themselves act as receptors for viruses, such as Galactosylceramide for human immunodeficiency virus (HIV). In addition, sphingolipids and their metabolites are inseparably interwoven in signal transduction processes, dynamic alterations of the cytoskeleton, and the regulation of innate and intrinsic responses of infected target cells. Depending on the nature of the intracellular pathogen, they may support or inhibit infections. Understanding of the underlying mechanisms depending on the specific virus, immune control, and type of disease may open new avenues for therapeutic interventions.
MeSH term(s)	Animals ; Antiviral Agents/pharmacology ; Drug Design ; Host-Pathogen Interactions ; Humans ; Signal Transduction/drug effects ; Sphingolipids/metabolism ; Virus Diseases/drug therapy ; Virus Diseases/metabolism ; Virus Diseases/virology ; Virus Internalization ; Virus Replication ; Viruses/drug effects ; Viruses/pathogenicity
Chemical Substances	Antiviral Agents ; Sphingolipids
Language	English
Publishing date	2013
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ISSN	0171-2004
ISSN	0171-2004
DOI	10.1007/978-3-7091-1511-4_16
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Article ; Online: Azido-Ceramides, a Tool to Analyse SARS-CoV-2 Replication and Inhibition-SARS-CoV-2 Is Inhibited by Ceramides.

Brenner, Daniela / Geiger, Nina / Schlegel, Jan / Diesendorf, Viktoria / Kersting, Louise / Fink, Julian / Stelz, Linda / Schneider-Schaulies, Sibylle / Sauer, Markus / Bodem, Jochen / Seibel, Jürgen

International journal of molecular sciences

2023 Volume 24, Issue 8

Abstract: Recently, we have shown that C6-ceramides efficiently suppress viral replication by trapping the virus in lysosomes. Here, we use antiviral assays to evaluate a synthetic ceramide derivative α-NH2-ω-N3-C6-ceramide (AKS461) and to confirm the biological ... ...

Abstract	Recently, we have shown that C6-ceramides efficiently suppress viral replication by trapping the virus in lysosomes. Here, we use antiviral assays to evaluate a synthetic ceramide derivative α-NH2-ω-N3-C6-ceramide (AKS461) and to confirm the biological activity of C6-ceramides inhibiting SARS-CoV-2. Click-labeling with a fluorophore demonstrated that AKS461 accumulates in lysosomes. Previously, it has been shown that suppression of SARS-CoV-2 replication can be cell-type specific. Thus, AKS461 inhibited SARS-CoV-2 replication in Huh-7, Vero, and Calu-3 cells up to 2.5 orders of magnitude. The results were confirmed by CoronaFISH, indicating that AKS461 acts comparable to the unmodified C6-ceramide. Thus, AKS461 serves as a tool to study ceramide-associated cellular and viral pathways, such as SARS-CoV-2 infections, and it helped to identify lysosomes as the central organelle of C6-ceramides to inhibit viral replication.
MeSH term(s)	Humans ; SARS-CoV-2/metabolism ; COVID-19 ; Ceramides/pharmacology ; Ceramides/metabolism ; Virus Replication ; Antiviral Agents/pharmacology
Chemical Substances	N-caproylsphingosine (038753E78J) ; Ceramides ; Antiviral Agents
Language	English
Publishing date	2023-04-14
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms24087281
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Article ; Online: Sphingolipids: Effectors and Achilles Heals in Viral Infections?

Schneider-Schaulies, Sibylle / Schumacher, Fabian / Wigger, Dominik / Schöl, Marie / Waghmare, Trushnal / Schlegel, Jan / Seibel, Jürgen / Kleuser, Burkhard

Cells

2021 Volume 10, Issue 9

Abstract: As viruses are obligatory intracellular parasites, any step during their life cycle strictly depends on successful interaction with their particular host cells. In particular, their interaction with cellular membranes is of crucial importance for most ... ...

Abstract	As viruses are obligatory intracellular parasites, any step during their life cycle strictly depends on successful interaction with their particular host cells. In particular, their interaction with cellular membranes is of crucial importance for most steps in the viral replication cycle. Such interactions are initiated by uptake of viral particles and subsequent trafficking to intracellular compartments to access their replication compartments which provide a spatially confined environment concentrating viral and cellular components, and subsequently, employ cellular membranes for assembly and exit of viral progeny. The ability of viruses to actively modulate lipid composition such as sphingolipids (SLs) is essential for successful completion of the viral life cycle. In addition to their structural and biophysical properties of cellular membranes, some sphingolipid (SL) species are bioactive and as such, take part in cellular signaling processes involved in regulating viral replication. It is especially due to the progress made in tools to study accumulation and dynamics of SLs, which visualize their compartmentalization and identify interaction partners at a cellular level, as well as the availability of genetic knockout systems, that the role of particular SL species in the viral replication process can be analyzed and, most importantly, be explored as targets for therapeutic intervention.
MeSH term(s)	Biological Transport ; Cell Membrane/chemistry ; Ceramides/metabolism ; Drug Delivery Systems ; HIV/growth & development ; Host Microbial Interactions ; Intracellular Membranes/chemistry ; SARS-CoV-2/growth & development ; Sphingolipids/metabolism ; Virion ; Virus Diseases ; Virus Replication ; Viruses/growth & development
Chemical Substances	Ceramides ; Sphingolipids
Language	English
Publishing date	2021-08-24
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells10092175
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Article: Use of Acid Ceramidase and Sphingosine Kinase Inhibitors as Antiviral Compounds Against Measles Virus Infection of Lymphocytes

Grafen, Anika / Schumacher, Fabian / Chithelen, Janice / Kleuser, Burkhard / Beyersdorf, Niklas / Schneider-Schaulies, Jürgen

Frontiers in cell and developmental biology

2019 Volume 7, Page(s) 218

Abstract: As structural membrane components and signaling effector molecules sphingolipids influence a plethora of host cell functions, and by doing so also the replication of viruses. Investigating the effects of various inhibitors of sphingolipid metabolism in ... ...

Abstract	As structural membrane components and signaling effector molecules sphingolipids influence a plethora of host cell functions, and by doing so also the replication of viruses. Investigating the effects of various inhibitors of sphingolipid metabolism in primary human peripheral blood lymphocytes (PBL) and the human B cell line BJAB we found that not only the sphingosine kinase (SphK) inhibitor SKI-II, but also the acid ceramidase inhibitor ceranib-2 efficiently inhibited measles virus (MV) replication. Virus uptake into the target cells was not grossly altered by the two inhibitors, while titers of newly synthesized MV were reduced by approximately 1 log (90%) in PBL and 70-80% in BJAB cells. Lipidomic analyses revealed that in PBL SKI-II led to increased ceramide levels, whereas in BJAB cells ceranib-2 increased ceramides. SKI-II treatment decreased sphingosine-1-phosphate (S1P) levels in PBL and BJAB cells. Furthermore, we found that MV infection of lymphocytes induced a transient (0.5-6 h) increase in S1P, which was prevented by SKI-II. Investigating the effect of the inhibitors on the metabolic (mTORC1) activity we found that ceranib-2 reduced the phosphorylation of p70 S6K in PBL, and that both inhibitors, ceranib-2 and SKI-II, reduced the phosphorylation of p70 S6K in BJAB cells. As mTORC1 activity is required for efficient MV replication, this effect of the inhibitors is one possible antiviral mechanism. In addition, reduced intracellular S1P levels affect a number of signaling pathways and functions including Hsp90 activity, which was reported to be required for MV replication. Accordingly, we found that pharmacological inhibition of Hsp90 with the inhibitor 17-AAG strongly impaired MV replication in primary PBL. Thus, our data suggest that treatment of lymphocytes with both, acid ceramidase and SphK inhibitors, impair MV replication by affecting a number of cellular activities including mTORC1 and Hsp90, which alter the metabolic state of the cells causing a hostile environment for the virus.
Language	English
Publishing date	2019-10-01
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2737824-X
ISSN	2296-634X
ISSN	2296-634X
DOI	10.3389/fcell.2019.00218
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