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Maria Moysidou, Sevasti Karaliota, Elisavet Kodela, Maria Salagianni, Yassemi Koutmani, Antonia Katsouda, Konstantia Kodella, Panagiotis Tsakanikas, Styliani Ourailidou, Evangelos Andreakos, Nikolaos Kostomitsopoulos, Dimitris Skokos, Antonios Chatzigeorgiou, Kyoung-Jin Chung, Stefan Bornstein, Mark W Sleeman, Triantafyllos Chavakis, Katia P Karalis
Although accumulation of lymphocytes in the white adipose tissue (WAT) in obesity is linked to insulin resistance, it remains unclear whether lymphocytes also participate in the regulation of energy homeostasis in the WAT. Here, we demonstrate enhanced energy dissipation in Rag1-/- mice, increased catecholaminergic input to subcutaneous WAT, and significant beige adipogenesis. Adoptive transfer experiments demonstrated that CD8+ T cell deficiency accounts for the enhanced beige adipogenesis in Rag1-/- mice...
March 8, 2018: JCI Insight
Siroon Bekkering, Rob J W Arts, Boris Novakovic, Ioannis Kourtzelis, Charlotte D C C van der Heijden, Yang Li, Calin D Popa, Rob Ter Horst, Julia van Tuijl, Romana T Netea-Maier, Frank L van de Veerdonk, Triantafyllos Chavakis, Leo A B Joosten, Jos W M van der Meer, Henk Stunnenberg, Niels P Riksen, Mihai G Netea
Innate immune cells can develop long-term memory after stimulation by microbial products during infections or vaccinations. Here, we report that metabolic signals can induce trained immunity. Pharmacological and genetic experiments reveal that activation of the cholesterol synthesis pathway, but not the synthesis of cholesterol itself, is essential for training of myeloid cells. Rather, the metabolite mevalonate is the mediator of training via activation of IGF1-R and mTOR and subsequent histone modifications in inflammatory pathways...
January 11, 2018: Cell
V I Alexaki, G Fodelianaki, A Neuwirth, C Mund, A Kourgiantaki, E Ieronimaki, K Lyroni, M Troullinaki, C Fujii, W Kanczkowski, A Ziogas, M Peitzsch, S Grossklaus, B Sönnichsen, A Gravanis, S R Bornstein, I Charalampopoulos, C Tsatsanis, T Chavakis
Dehydroepiandrosterone (DHEA) is the most abundant circulating steroid hormone in humans, produced by the adrenals, the gonads and the brain. DHEA was previously shown to bind to the nerve growth factor receptor, tropomyosin-related kinase A (TrkA), and to thereby exert neuroprotective effects. Here we show that DHEA reduces microglia-mediated inflammation in an acute lipopolysaccharide-induced neuro-inflammation model in mice and in cultured microglia in vitro. DHEA regulates microglial inflammatory responses through phosphorylation of TrkA and subsequent activation of a pathway involving Akt1/Akt2 and cAMP response element-binding protein...
September 12, 2017: Molecular Psychiatry
Thati Madhusudhan, Hongjie Wang, Sanchita Ghosh, Wei Dong, Varun Kumar, Moh'd Mohanad Al-Dabet, Jayakumar Manoharan, Sumra Nazir, Ahmed Elwakiel, Fabian Bock, Shrey Kohli, Andi Marquardt, Ibrahim Sögüt, Khurrum Shahzad, Andreas J Müller, Charles T Esmon, Peter P Nawroth, Jochen Reiser, Triantafyllos Chavakis, Wolfram Ruf, Berend Isermann
Coagulation proteases have increasingly recognized functions beyond hemostasis and thrombosis. Disruption of activated protein C (aPC) or insulin signaling impair function of podocytes and ultimately cause dysfunction of the glomerular filtration barrier and diabetic kidney disease (DKD). We here show that insulin and aPC converge on a common spliced-X-box binding protein-1 (sXBP1) signaling pathway to maintain endoplasmic reticulum (ER) homeostasis. Analogous to insulin, physiological levels of aPC maintain ER proteostasis in DKD...
September 21, 2017: Blood
Themis Alissafi, Aggelos Banos, Louis Boon, Tim Sparwasser, Alessandra Ghigo, Kajsa Wing, Dimitrios Vassilopoulos, Dimitrios Boumpas, Triantafyllos Chavakis, Ken Cadwell, Panayotis Verginis
Design of efficacious Treg-based therapies and establishment of clinical tolerance in autoimmune diseases have proven to be challenging. The clinical implementation of Treg immunotherapy has been hampered by various impediments related to the stability and isolation procedures of Tregs as well as the specific in vivo targets of Treg modalities. Herein, we have demonstrated that Foxp3+ Tregs potently suppress autoimmune responses in vivo through inhibition of the autophagic machinery in DCs in a cytotoxic T-lymphocyte-associated protein 4-dependent (CTLA4-dependent) manner...
June 30, 2017: Journal of Clinical Investigation
Holger Garn, Sabine Bahn, Bernhard T Baune, Elisabeth B Binder, Hans Bisgaard, Talal A Chatila, Triantafyllos Chavakis, Carsten Culmsee, Udo Dannlowski, Steffen Gay, James Gern, Tari Haahtela, Tilo Kircher, Ulf Müller-Ladner, Markus F Neurath, Klaus T Preissner, Christoph Reinhardt, Graham Rook, Shannon Russell, Bernd Schmeck, Thaddeus Stappenbeck, Ulrich Steinhoff, Jim van Os, Scott Weiss, Michael Zemlin, Harald Renz
Recent research indicates that chronic inflammatory diseases, including allergies and autoimmune and neuropsychiatric diseases, share common pathways of cellular and molecular dysregulation. It was the aim of the International von-Behring-Röntgen Symposium (October 16-18, 2014, in Marburg, Germany) to discuss recent developments in this field. These include a concept of biodiversity; the contribution of urbanization, lifestyle factors, and nutrition (eg, vitamin D); and new mechanisms of metabolic and immune dysregulation, such as extracellular and intracellular RNAs and cellular and mitochondrial stress...
July 2016: Journal of Allergy and Clinical Immunology
Erik J M Toonen, Andreea-Manuela Mirea, Cees J Tack, Rinke Stienstra, Dov B Ballak, Janna A van Diepen, Anneke Hijmans, Triantafyllos Chavakis, Wim H Dokter, Christine T N Pham, Mihai G Netea, Charles A Dinarello, Leo A B Joosten
Activation of inflammatory pathways is known to accompany development of obesity-induced non-alcoholic fatty liver disease (NAFLD), insulin resistance and type 2 diabetes. In addition to caspase-1, the neutrophil serine proteases proteinase 3, neutrophil elastase and cathepsin G are able to process the inactive pro-inflammatory mediators IL-1β and IL-18 to their bioactive forms, thereby regulating inflammatory responses. In the present study, we investigated whether proteinase 3 is involved in obesity-induced development of insulin resistance and NAFLD...
May 24, 2016: Molecular Medicine
Kerstin Göbel, Susann Pankratz, Chloi-Magdalini Asaridou, Alexander M Herrmann, Stefan Bittner, Monika Merker, Tobias Ruck, Sarah Glumm, Friederike Langhauser, Peter Kraft, Thorsten F Krug, Johanna Breuer, Martin Herold, Catharina C Gross, Denise Beckmann, Adelheid Korb-Pap, Michael K Schuhmann, Stefanie Kuerten, Ioannis Mitroulis, Clemens Ruppert, Marc W Nolte, Con Panousis, Luisa Klotz, Beate Kehrel, Thomas Korn, Harald F Langer, Thomas Pap, Bernhard Nieswandt, Heinz Wiendl, Triantafyllos Chavakis, Christoph Kleinschnitz, Sven G Meuth
Aberrant immune responses represent the underlying cause of central nervous system (CNS) autoimmunity, including multiple sclerosis (MS). Recent evidence implicated the crosstalk between coagulation and immunity in CNS autoimmunity. Here we identify coagulation factor XII (FXII), the initiator of the intrinsic coagulation cascade and the kallikrein-kinin system, as a specific immune cell modulator. High levels of FXII activity are present in the plasma of MS patients during relapse. Deficiency or pharmacologic blockade of FXII renders mice less susceptible to experimental autoimmune encephalomyelitis (a model of MS) and is accompanied by reduced numbers of interleukin-17A-producing T cells...
May 18, 2016: Nature Communications
Kenneth Peuker, Stefanie Muff, Jun Wang, Sven Künzel, Esther Bosse, Yvonne Zeissig, Giuseppina Luzzi, Marijana Basic, Anne Strigli, Andrea Ulbricht, Arthur Kaser, Alexander Arlt, Triantafyllos Chavakis, Gijs R van den Brink, Clemens Schafmayer, Jan-Hendrik Egberts, Thomas Becker, Marco E Bianchi, André Bleich, Christoph Röcken, Jochen Hampe, Stefan Schreiber, John F Baines, Richard S Blumberg, Sebastian Zeissig
Inflammation-associated pathways are active in intestinal epithelial cells (IECs) and contribute to the pathogenesis of colorectal cancer (CRC). Calcineurin, a phosphatase required for the activation of the nuclear factor of activated T cells (NFAT) family of transcription factors, shows increased expression in CRC. We therefore investigated the role of calcineurin in intestinal tumor development. We demonstrate that calcineurin and NFAT factors are constitutively expressed by primary IECs and selectively activated in intestinal tumors as a result of impaired stratification of the tumor-associated microbiota and toll-like receptor signaling...
May 2016: Nature Medicine
Marina Nati, David Haddad, Andreas L Birkenfeld, Christian A Koch, Triantafyllos Chavakis, Antonios Chatzigeorgiou
The low grade inflammatory state present in obesity promotes the progression of Non-Alcoholic Fatty Liver Disease (NAFLD). In Non-Alcoholic Steatohepatitis (NASH), augmented hepatic steatosis is accompanied by aberrant intrahepatic inflammation and exacerbated hepatocellular injury. NASH is an important disorder and can lead to fibrosis, cirrhosis and even neoplasia. The pathology of NASH involves a complex network of mechanisms, including increased infiltration of different subsets of immune cells, such as monocytes, T-lymphocytes and neutrophils, to the liver, as well as activation and in situ expansion of liver resident cells such as Kupffer cells or stellate cells...
March 2016: Reviews in Endocrine & Metabolic Disorders
Matina Economopoulou, Nemanja Avramovic, Anne Klotzsche-von Ameln, Irina Korovina, David Sprott, Maryna Samus, Bettina Gercken, Maria Troullinaki, Sylvia Grossklaus, Richard H Funk, Xuri Li, Beat A Imhof, Valeria V Orlova, Triantafyllos Chavakis
In proliferative retinopathies, like proliferative diabetic retinopathy and retinopathy of prematurity (ROP), the hypoxia response is sustained by the failure of the retina to revascularise its ischaemic areas. Non-resolving retina ischaemia/hypoxia results in upregulation of pro-angiogenic factors and pathologic neovascularisation with ectopic, fragile neovessels. Promoting revascularisation of the retinal avascular area could interfere with this vicious cycle and lead to vessel normalisation. Here, we examined the function of endothelial junctional adhesion molecule-C (JAM-C) in the context of ROP...
November 25, 2015: Thrombosis and Haemostasis
Osama A Hamad, Ioannis Mitroulis, Karin Fromell, Huda Kozarcanin, Triantafyllos Chavakis, Daniel Ricklin, John D Lambris, Kristina N Ekdahl, Bo Nilsson
Complement component C3 has a potential role in thrombotic pathologies. It is transformed, without proteolytic cleavage, into C3(H2O) upon binding to the surface of activated platelets. We hypothesise that C3(H2O) bound to activated platelets and to platelet-derived microparticles (PMPs) contributes to platelet-PMN complex (PPC) formation and to the binding of PMPs to PMNs. PAR-1 activation of platelets in human whole blood from normal individuals induced the formation of CD16+/CD42a+ PPC. The complement inhibitor compstatin and a C5a receptor antagonist inhibited PPC formation by 50 %, while monoclonal antibodies to C3(H2O) or anti-CD11b inhibited PPC formation by 75-100 %...
November 25, 2015: Thrombosis and Haemostasis
E Baraban, T Chavakis, B S Hamilton, S Sales, M Wabitsch, S R Bornstein, M Ehrhart-Bornstein
BACKGROUND: Obesity is characterized by increased adipocyte number and size as well as white adipose tissue (WAT) inflammation, which is fundamental for the development of insulin resistance and type-2 diabetes. These processes, regulated by various endocrine, paracrine and autocrine factors, are extensively studied with the hope to interfere and to inhibit weight gain and related complications in obese patients. Recent data suggest an important role of bone morphogenic protein 4 (BMP4) in the regulation of adipogenesis and development of obesity...
February 2016: International Journal of Obesity: Journal of the International Association for the Study of Obesity
Antonios Chatzigeorgiou, Triantafyllos Chavakis
Low-grade inflammation in the obese AT (AT) and the liver is a critical player in the development of obesity-related metabolic dysregulation, including insulin resistance, type 2 diabetes and non-alcoholic steatohepatitis (NASH). Myeloid as well as lymphoid cells infiltrate the AT and the liver and expand within these metabolic organs as a result of excessive nutrient intake, thereby exacerbating tissue inflammation. Macrophages are the paramount cell population in the field of metabolism-related inflammation; as obesity progresses, a switch takes place within the AT environment from an M2-alternatively activated macrophage state to an M1-inflammatory macrophage-dominated milieu...
2016: Handbook of Experimental Pharmacology
B Reichart, H Niemann, T Chavakis, J Denner, E Jaeckel, B Ludwig, G Marckmann, A Schnieke, R Schwinzer, J Seissler, R R Tönjes, N Klymiuk, E Wolf, S R Bornstein
Solid organ and cell transplantation, including pancreatic islets constitute the treatment of choice for chronic terminal diseases. However, the clinical use of allogeneic transplantation is limited by the growing shortage of human organs. This has prompted us to initiate a unique multi-center and multi-team effort to promote translational research in xenotransplantation to bring xenotransplantation to the clinical setting. Supported by the German Research Foundation, an interdisciplinary group of surgeons, internal medicine doctors, diabetologists, material sciences experts, immunologists, cell biologists, virologists, veterinarians, and geneticists have established a collaborative research center (CRC) focusing on the biology of xenogeneic cell, tissue, and organ transplantation...
January 2015: Hormone and Metabolic Research, Hormon- und Stoffwechselforschung, Hormones et Métabolisme
Tom Seijkens, Pascal Kusters, Antonios Chatzigeorgiou, Triantafyllos Chavakis, Esther Lutgens
In the past two decades, numerous experimental and clinical studies have established the importance of inflammation and immunity in the development of obesity and its metabolic complications, including insulin resistance and type 2 diabetes mellitus. In this context, T cells orchestrate inflammatory processes in metabolic organs, such as the adipose tissue (AT) and liver, thereby mediating obesity-related metabolic deterioration. Costimulatory molecules, which are present on antigen-presenting cells and naïve T cells in the AT, are known to mediate the crosstalk between the adaptive and innate immune system and to direct T-cell responses in inflammation...
December 2014: Diabetes
Eun Young Choi, Jong-Hyung Lim, Ales Neuwirth, Matina Economopoulou, Antonios Chatzigeorgiou, Kyoung-Jin Chung, Stefan Bittner, Seung-Hwan Lee, Harald Langer, Maryna Samus, Hyesoon Kim, Geum-Sil Cho, Tjalf Ziemssen, Khalil Bdeir, Emmanouil Chavakis, Jae-Young Koh, Louis Boon, Kavita Hosur, Stefan R Bornstein, Sven G Meuth, George Hajishengallis, Triantafyllos Chavakis
Inflammation in the central nervous system (CNS) and disruption of its immune privilege are major contributors to the pathogenesis of multiple sclerosis (MS) and of its rodent counterpart, experimental autoimmune encephalomyelitis (EAE). We have previously identified developmental endothelial locus-1 (Del-1) as an endogenous anti-inflammatory factor, which inhibits integrin-dependent leukocyte adhesion. Here we show that Del-1 contributes to the immune privilege status of the CNS. Intriguingly, Del-1 expression decreased in chronic-active MS lesions and in the inflamed CNS in the course of EAE...
July 2015: Molecular Psychiatry
S Rahmig, S R Bornstein, T Chavakis, E Jaeckel, C Waskow
We comment here on the suitability of available mouse models for type 1 diabetes research including research on therapeutic pancreatic islet transplantation. The major emphasis will be laid on models that require minimal invasive procedures. Most biological processes are too complex for a complete recapitulation in a test tube. The study of innate or even adaptive immune responses involves a number of different cell types and organs making in vitro studies unreliable but also providing extreme challenges for the use of surrogate model organisms...
January 2015: Hormone and Metabolic Research, Hormon- und Stoffwechselforschung, Hormones et Métabolisme
M M Swierczynska, I Mateska, M Peitzsch, S R Bornstein, T Chavakis, G Eisenhofer, V Lamounier-Zepter, S Eaton
BACKGROUND/OBJECTIVES: Obesity is a major risk factor for the development of type 2 diabetes and other debilitating diseases. Obesity and diabetes are intimately linked with altered levels of adrenal steroids. Elevated levels of these hormones induce insulin resistance and cause cardiovascular diseases. The mechanisms underlying obesity-related alterations in adrenal steroids are still not well understood. Here, we investigated how diet-induced obesity affects the morphology and function of the mouse adrenal cortex...
February 2015: International Journal of Obesity: Journal of the International Association for the Study of Obesity
Antonios Chatzigeorgiou, Kyoung-Jin Chung, Ruben Garcia-Martin, Vasileia-Ismini Alexaki, Anne Klotzsche-von Ameln, Julia Phieler, David Sprott, Waldemar Kanczkowski, Theodora Tzanavari, Mohktar Bdeir, Sibylle Bergmann, Marc Cartellieri, Michael Bachmann, Polyxeni Nikolakopoulou, Andreas Androutsellis-Theotokis, Gabriele Siegert, Stefan R Bornstein, Michael H Muders, Louis Boon, Katia P Karalis, Esther Lutgens, Triantafyllos Chavakis
UNLABELLED: The low-grade inflammatory state present in obesity contributes to obesity-related metabolic dysregulation, including nonalcoholic steatohepatitis (NASH) and insulin resistance. Intercellular interactions between immune cells or between immune cells and hepatic parenchymal cells contribute to the exacerbation of liver inflammation and steatosis in obesity. The costimulatory molecules, B7.1 and B7.2, are important regulators of cell-cell interactions in several immune processes; however, the role of B7 costimulation in obesity-related liver inflammation is unknown...
October 2014: Hepatology: Official Journal of the American Association for the Study of Liver Diseases
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