ORCID Profile
0000-0003-3487-362X
Current Organisation
University of Veterinary Medicine Vienna
Does something not look right? The information on this page has been harvested from data sources that may not be up to date. We continue to work with information providers to improve coverage and quality. To report an issue, use the Feedback Form.
Publisher: MDPI AG
Date: 29-07-2022
DOI: 10.3390/NU14153120
Abstract: The rate of gut inflammatory diseases is growing in modern society. Previously, we showed that caloric restriction (CR) shapes gut microbiota composition and diminishes the expression of inflammatory factors along the gastrointestinal (GI) tract. The current project aimed to assess whether prominent dietary restrictive approaches, including intermittent fasting (IF), fasting-mimicking diet (FMD), and ketogenic diet (KD) have a similar effect as CR. We sought to verify which of the restrictive dietary approaches is the most potent and if the molecular pathways responsible for the impact of the diets overlap. We characterized the impact of the diets in the context of several dietary restriction-related parameters, including immune status in the GI tract microbiota and its metabolites bile acids (BAs) gut morphology as well as autophagy-, mitochondria-, and energy restriction-related parameters. The effects of the various diets are very similar, particularly between CR, IF, and FMD. The occurrence of a 50 kDa truncated form of occludin, the composition of the microbiota, and BAs distinguished KD from the other diets. Based on the results, we were able to provide a comprehensive picture of the impact of restrictive diets on the gut, indicating that restrictive protocols aimed at improving gut health may be interchangeable.
Publisher: Elsevier BV
Date: 03-2020
Publisher: Impact Journals, LLC
Date: 08-08-2017
Publisher: Wiley
Date: 08-10-2018
DOI: 10.1111/EPI.14573
Abstract: There exists solid evidence that endogenous galanin and galanin agonists exert anticonvulsive actions mediated both by galanin 1 receptor (GAL1‐R) and galanin 2 receptor (GAL2‐R). We have now investigated whether depletion of the recently identified third galanin receptor, GAL3‐R, and that of GAL2‐R, alters the threshold to the systemically applied γ‐aminobutyric acid (GABA) antagonist pentylenetetrazole (PTZ) or to intrahippoc ally administered kainic acid (KA). In neither model, GAL3‐KO mice differed in their latency to the first seizure, mean seizure duration, total number of seizures, or time spent in seizures compared to wild‐type controls. In addition, consistent with previous data, the response to PTZ was not altered in GAL2‐KO mice. In contrast, intrahippoc al KA resulted in a significantly increased number of seizures and time spent in seizures in GAL2‐KO mice, although the latency to the first seizure and the duration of in idual seizures was not altered. These results are consistent with the previous data showing that GAL2‐R knockdown does not affect the number of perforant path stimulations required for initiating status epilepticus but significantly increases the seizure severity during the ongoing status. In conclusion, our data support a specific role of GAL2‐R but not of GAL3‐R in mediating the anticonvulsive actions of endogenous galanin.
Publisher: MDPI AG
Date: 04-2021
DOI: 10.3390/MOLECULES26071978
Abstract: The neuropeptide galanin (GAL), which is expressed in limbic brain structures, has a strong impact on the regulation of mood and behavior. GAL exerts its effects via three G protein-coupled receptors (GAL1–3-R). Little is known about the effects of aging and loss of GAL-Rs on hippoc al-mediated processes connected to neurogenesis, such as learning, memory recall and anxiety, and cell proliferation and survival in the dorsal dentate gyrus (dDG) in mice. Our results demonstrate that loss of GAL3-R, but not GAL2-R, slowed learning and induced anxiety in older (12–14-month-old) mice. Lack of GAL2-R increased cell survival (BrdU incorporation) in the dDG of young mice. However, normal neurogenesis was observed in vitro using neural stem and precursor cells obtained from GAL2-R and GAL3-R knockouts upon GAL treatment. Interestingly, we found sub-strain differences between C57BL/6J and C57BL/6N mice, the latter showing faster learning, less anxiety and lower cell survival in the dDG. We conclude that GAL-R signaling is involved in cognitive functions and can modulate the survival of cells in the neurogenic niche, which might lead to new therapeutic applications. Furthermore, we observed that the mouse sub-strain had a profound impact on the behavioral parameters analyzed and should therefore be carefully considered in future studies.
Publisher: Elsevier BV
Date: 10-2019
DOI: 10.1016/J.PEPTIDES.2018.08.010
Abstract: Antibodies are an integral biomedical tool, not only for research but also as therapeutic agents. However, progress can only be made with sensitive and specific antibodies. The regulatory (neuro)peptide galanin and its three endogenous receptors (GAL
Publisher: Impact Journals, LLC
Date: 17-07-2017
Publisher: Proceedings of the National Academy of Sciences
Date: 29-04-2014
Abstract: In the modern world, stress-related diseases, including depression and anxiety disorders, are rapidly increasing. Neuropeptides are important modulators of these diseases. The neuropeptide galanin (GAL) has already been implicated in anxiety- and depression-related behaviors, but the relevant receptor subtypes remain to be elucidated. In the present work, we are the first, to our knowledge, to examine the role of the GAL 3 receptor in anxiety- and depression-related behaviors in GAL 3 receptor -deficient mice. We provide evidence that this receptor subtype is involved in stress-related diseases, and we propose this receptor as a target for alternative treatment strategies for mood disorders.
Publisher: Elsevier BV
Date: 2018
DOI: 10.1016/J.JID.2017.08.015
Abstract: The neuropeptide galanin is distributed in the central and peripheral nervous systems and in non-neuronal peripheral organs, including the skin. Galanin acts via three G protein-coupled receptors which, except galanin receptor 1, are expressed in various skin structures. The galanin system has been associated with inflammatory processes of the skin and of several other organs. Psoriasis is an inflammatory skin disease with increased neovascularization, keratinocyte hyperproliferation, a proinflammatory cytokine milieu, and immune cell infiltration. In this study, we showed that galanin receptor 3 is present in endothelial cells in human and murine dermal vessels and is co-expressed with nestin in neo-vessels of psoriatic patients. Moreover, in a murine psoriasis model, we showed that C57/BL6 mice lacking galanin receptor 3 display a milder course of psoriasis upon imiquimod treatment, leading to decreased disease severity, delayed neo-vascularization, reduced infiltration of neutrophils, and significantly lower levels of proinflammatory cytokines compared with wild-type mice. In contrast, galanin receptor 2-knockout animals did not differ significantly from wild type mice at both the macroscopic and molecular levels in their inflammatory response to imiquimod treatment. Our data indicate that galanin receptor 3, but not galanin receptor 2, plays an important role in psoriasis-like skin inflammation.
Publisher: Springer Science and Business Media LLC
Date: 03-03-2016
DOI: 10.1007/S12031-016-0732-9
Abstract: Neurogenic inflammation mediated by peptidergic sensory nerves has a crucial impact on the pathogenesis of various joint diseases. Galanin is a regulatory sensory neuropeptide, which has been shown to attenuate neurogenic inflammation, modulate neutrophil activation, and be involved in the development of adjuvant arthritis, but our current understanding about its targets and physiological importance is incomplete. Among the receptors of galanin (GAL 1 – 3 ), GAL 3 has been found to be the most abundantly expressed in the vasculature and on the surface of some immune cells. However, since there are minimal in vivo data on the role of GAL 3 in joint diseases, we analyzed its involvement in different inflammatory mechanisms of the K/BxN serum transfer-model of autoimmune arthritis employing GAL 3 gene-deficient mice. After arthritis induction, GAL 3 knockouts demonstrated increased clinical disease severity and earlier hindlimb edema than wild types. Vascular hyperpermeability determined by in vivo fluorescence imaging was also elevated compared to the wild-type controls. However, neutrophil accumulation detected by in vivo luminescence imaging or arthritic mechanical hyperalgesia was not altered by the lack of the GAL 3 receptor. Our findings suggest that GAL 3 has anti-inflammatory properties in joints by inhibiting vascular hyperpermeability and consequent edema formation.
Publisher: Elsevier BV
Date: 04-2016
DOI: 10.1016/J.NPEP.2015.12.003
Abstract: Galanin and its receptors (GAL1, GAL2, GAL3) modulate a range of neuronal, immune and vascular activities. In vivo administration of SNAP 37889 (1-phenyl-3-[[3-(trifluoromethyl)phenyl]imino]-1H-indol-2-one), a potent small non-peptidergic antagonist of GAL3, was reported to reduce anxiety- and depression-related behavior, ethanol consumption, and antagonizes the effect of galanin on plasma extravasation in rodent models. Accordingly, SNAP 37889 has been proposed as a potential therapeutic agent to treat anxiety and depression disorders. Therefore, we evaluated the toxicity of SNAP 37889 to different cell types. Our experiments revealed that SNAP 37889 (≥10μM) induced apoptosis in epithelial (HMCB) and microglial (BV-2) cell lines expressing endogenous GAL3, in peripheral blood mononuclear cells and promyelocytic leukemia cells (HL-60) expressing GAL2, and in a neuronal cell line (SH-SY5Y) lacking galanin receptor expression altogether. In conclusion, SNAP 37889 is toxic to a variety of cell types independent of GAL3 expression. We caution that the clinical use of SNAP 37889 at doses that might be used to treat anxiety- or depression- related diseases could have unexpected non-galanin receptor-mediated toxicity, especially on immune cells.
Publisher: Springer Science and Business Media LLC
Date: 12-06-2015
Publisher: Wiley
Date: 07-01-2015
DOI: 10.1111/APHA.12444
Abstract: Polymorphonuclear neutrophils are key players in innate immunity. The innate immune system needs to be tightly controlled to ensure proper activation but also no overactivation. Galanin has been shown to regulate inflammatory reactions, and therefore, we aimed to elucidate the expression of galanin and its three receptors ( GAL 1 ‐ GAL 3 ) in polymorphonuclear neutrophils and to evaluate whether galanin exerts direct or indirect effects on human and murine polymorphonuclear neutrophils. Human peripheral polymorphonuclear neutrophils were isolated from fresh blood of healthy donors, and murine polymorphonuclear neutrophils were isolated from bone marrow of C57 BL /6N mice. Gene expression was evaluated by qRT ‐ PCR . As a marker for polymorphonuclear neutrophil activation, CD 11b integrin surface expression was measured by FACS analysis. Furthermore, a label‐free technology measuring ligand‐induced dynamic mass redistribution was used to evaluate the response of polymorphonuclear neutrophils to galanin. GAL 2 receptor expression was found in both human and murine polymorphonuclear neutrophils, galanin and GAL 3 receptor were exclusively expressed in murine bone marrow polymorphonuclear neutrophils, and GAL 1 receptor was not detectable in polymorphonuclear neutrophils of either species. Galanin treatment was not able to induce CD 11b integrin surface expression or dynamic mass redistribution in human polymorphonuclear neutrophils and murine bone marrow polymorphonuclear neutrophils. However, galanin treatment significantly enhanced the response of polymorphonuclear neutrophils of both species to interleukin‐8. Galanin can be regarded as an immunomodulatory peptide as it can sensitize polymorphonuclear neutrophils towards pro‐inflammatory cytokines in humans and mice.
Publisher: Springer Science and Business Media LLC
Date: 10-05-2019
DOI: 10.1038/S41598-019-43704-7
Abstract: The regulatory peptide galanin is broadly distributed in the central- and peripheral nervous systems as well as in non-neuronal tissues, where it exerts its erse physiological functions via three G-protein-coupled receptors (GAL 1-3 -R). Regulatory peptides are important mediators of the cross-communication between the nervous- and immune systems and have emerged as a focus of new therapeutics for a variety of inflammatory diseases. Studies on inflammatory animal models and immune cells revealed both pro- and anti-inflammatory functions of galanin. Here, we probed specific immune-related functions of the galanin system and found galanin and GAL 1 -R and GAL 2 -R mRNA to be expressed in a range of human immune cells. In particular, macrophages displayed differentiation- and polarization-dependent expression of galanin and its receptors. Exposure to exogenous galanin affected the cytokine/chemokine expression profile of macrophages differently, depending on their differentiation and polarization, and mainly modulated the expression of chemokines (CCL2, CCL3, CCL5 and CXCL8) and anti-inflammatory cytokines (TGF-β, IL-10 and IL-1Ra), especially in type-1 macrophages. Cytokine/chemokine expression levels in interferon-gamma- and lipopolysaccharide-polarized macrophages were upregulated whereas in unpolarized macrophages they were downregulated upon galanin treatment for 20 hours. This study illuminates the regulation of important cytokines/chemokines in macrophages by galanin, depending on specific cell activation.
No related grants have been discovered for Felix Sternberg.