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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...
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
E Y Choi, J-H Lim, A Neuwirth, M Economopoulou, A Chatzigeorgiou, K-J Chung, S Bittner, S-H Lee, H Langer, M Samus, H Kim, G-S Cho, T Ziemssen, K Bdeir, E Chavakis, J-Y Koh, L Boon, K Hosur, S R Bornstein, S G Meuth, G Hajishengallis, T 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
Niki M Moutsopoulos, Joanne Konkel, Mojgan Sarmadi, Mehmet A Eskan, Teresa Wild, Nicolas Dutzan, Loreto Abusleme, Camille Zenobia, Kavita B Hosur, Toshiharu Abe, Gulbu Uzel, Wanjun Chen, Triantafyllos Chavakis, Steven M Holland, George Hajishengallis
Leukocyte adhesion deficiency type I (LAD-I), a disease syndrome associated with frequent microbial infections, is caused by mutations on the CD18 subunit of β₂ integrins. LAD-I is invariably associated with severe periodontal bone loss, which historically has been attributed to the lack of neutrophil surveillance of the periodontal infection. We provide an alternative mechanism by showing that the cytokine interleukin-17 (IL-17) plays a major role in the oral pathology of LAD-I. Defective neutrophil recruitment in LAD-I patients or in LFA-1 (CD11a/CD18)-deficient mice--which exhibit the LAD-I periodontal phenotype--was associated with excessive production of predominantly T cell-derived IL-17 in the periodontal tissue, although innate lymphoid cells also contributed to pathological IL-17 elevation in the LFA-1-deficient mice...
March 26, 2014: Science Translational Medicine
Antonios Chatzigeorgiou, Tom Seijkens, Barbara Zarzycka, David Engel, Marjorie Poggi, Susan van den Berg, Sjoerd van den Berg, Oliver Soehnlein, Holger Winkels, Linda Beckers, Dirk Lievens, Ann Driessen, Pascal Kusters, Erik Biessen, Ruben Garcia-Martin, Anne Klotzsche-von Ameln, Marion Gijbels, Randolph Noelle, Louis Boon, Tilman Hackeng, Klaus-Martin Schulte, Klaus Schulte, Aimin Xu, Gert Vriend, Sander Nabuurs, Kyoung-Jin Chung, Ko Willems van Dijk, Patrick C N Rensen, Norbert Gerdes, Menno de Winther, Norman L Block, Andrew V Schally, Christian Weber, Stefan R Bornstein, Gerry Nicolaes, Triantafyllos Chavakis, Esther Lutgens
The immune system plays an instrumental role in obesity and insulin resistance. Here, we unravel the role of the costimulatory molecule CD40 and its signaling intermediates, TNF receptor-associated factors (TRAFs), in diet-induced obesity (DIO). Although not exhibiting increased weight gain, male CD40(-/-) mice in DIO displayed worsened insulin resistance, compared with wild-type mice. This worsening was associated with excessive inflammation of adipose tissue (AT), characterized by increased accumulation of CD8(+) T cells and M1 macrophages, and enhanced hepatosteatosis...
February 18, 2014: Proceedings of the National Academy of Sciences of the United States of America
J Graessler, T D Bornstein, D Goel, V P Bhalla, T Lohmann, T Wolf, M Koch, Y Qin, J Licinio, M-L Wong, T Chavakis, A Xu, A Shevchenko, K Schuhmann, P E H Schwarz, K-M Schulte, A Patel, S R Bornstein
Bariatric surgery is a well-established approach to improve metabolic disease in morbidly obese patients with high cardiovascular risk. The post-operative normalization of lipid metabolism has a central role in the prevention of future cardiovascular events. The aim of the present study therefore was to characterize changes of plasma lipidomic patterns, consisting of 229 lipid species of 13 lipid classes, 3 months after Roux-en-Y gastric bypass (RYGB) in morbidly obese patients with and without diabetes. RYGB resulted in a 15-32% decrease of body mass index, which was associated with a significant reduction of total cholesterol (TC, -28...
June 2014: Pharmacogenomics Journal
Ioannis Mitroulis, Yoon-Young Kang, Carl G Gahmberg, Gabriele Siegert, George Hajishengallis, Triantafyllos Chavakis, Eun-Young Choi
No abstract text is available yet for this article.
May 5, 2014: Thrombosis and Haemostasis
A Chatzigeorgiou, J Phieler, J Gebler, S R Bornstein, T Chavakis
Macrophages and lymphocytes are implicated in obesity-related adipose tissue inflammation via interactions with adipocytes. Co-stimulatory systems, especially the CD40-CD40L system, play an important role in T cell activation and inflammatory reactions. CD40L was recently shown to promote adipose tissue inflammation in vivo, yet, the mechanisms underlying its function in the intercellular communication between inflammatory cells and adipocytes remain not entirely clear. Here we found that adipocyte stimulation with CD40L increased the expression of CD40, as well as of chemokines, such as MCP-1, CCL4, or CCL5, whereas adipocyte CD40 expression was also stimulated by TNF but not palmitate...
September 2013: Hormone and Metabolic Research, Hormon- und Stoffwechselforschung, Hormones et Métabolisme
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