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  1. Article ; Online: Meloxicam treatment disrupts the regional structure of innate inflammation sites by targeting the pro-inflammatory effects of prostanoids.

    Schäufele, Tim J / Kolbinger, Anja / Friedel, Joschua / Gurke, Robert / Geisslinger, Gerd / Weigert, Andreas / Pierre, Sandra / Scholich, Klaus

    British journal of pharmacology

    2023  Volume 181, Issue 7, Page(s) 1051–1067

    Abstract: Background and purpose: Non-steroidal anti-inflammatory drugs (NSAIDs) are the most widely prescribed drugs in the world due to their analgesic, antipyretic and anti-inflammatory effects. However, NSAIDs inhibit prostanoid synthesis, interfering with ... ...

    Abstract Background and purpose: Non-steroidal anti-inflammatory drugs (NSAIDs) are the most widely prescribed drugs in the world due to their analgesic, antipyretic and anti-inflammatory effects. However, NSAIDs inhibit prostanoid synthesis, interfering with their pro-inflammatory and anti-inflammatory functions and potentially prolonging acute inflammation.
    Experimental approach: We used high-content immunohistochemistry to define the impact of meloxicam treatment on spatially separated pro-inflammatory and anti-inflammatory processes during innate inflammation in mice induced by zymosan. This allowed us to determine the effect of meloxicam treatment on the organization of pro-inflammatory and anti-inflammatory microenvironments, thereby identifying relevant changes in immune cell localization, recruitment and activation.
    Key results: Meloxicam treatment reduced zymosan-induced thermal hypersensitivity at early time points but delayed its resolution. High-content immunohistochemistry revealed that the pro-inflammatory area was smaller after treatment, diminishing neutrophil recruitment, M1-like macrophage polarization, and especially phagocytosis by neutrophils and macrophages. The polarization of macrophages towards the M2-like anti-inflammatory phenotype was unaffected, and the number of anti-inflammatory eosinophils actually increased.
    Conclusion and implications: High-content immunohistochemistry was able to identify relevant meloxicam-mediated effects on inflammatory processes based on alterations in the regional structure of inflammation sites. Meloxicam delayed the clearance of pathogens by inhibiting pro-inflammatory processes, causing prolonged inflammation. Our data suggest that the prescription of NSAIDs as a treatment during an acute pathogen-driven inflammation should be reconsidered in patients with compromised immune systems.
    MeSH term(s) Humans ; Mice ; Animals ; Meloxicam/adverse effects ; Prostaglandins ; Zymosan ; Thiazoles/pharmacology ; Thiazoles/therapeutic use ; Thiazines/pharmacology ; Thiazines/therapeutic use ; Anti-Inflammatory Agents, Non-Steroidal/adverse effects ; Inflammation/chemically induced ; Inflammation/drug therapy ; Anti-Inflammatory Agents/adverse effects
    Chemical Substances Meloxicam (VG2QF83CGL) ; Prostaglandins ; Zymosan (9010-72-4) ; Thiazoles ; Thiazines ; Anti-Inflammatory Agents, Non-Steroidal ; Anti-Inflammatory Agents
    Language English
    Publishing date 2023-11-22
    Publishing country England
    Document type Journal Article
    ZDB-ID 80081-8
    ISSN 1476-5381 ; 0007-1188
    ISSN (online) 1476-5381
    ISSN 0007-1188
    DOI 10.1111/bph.16261
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Uf I Zs.146: Show issues Location:
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  2. Article ; Online: Behind the Wall-Compartment-Specific Neovascularisation during Post-Stroke Recovery in Mice.

    Kolbinger, Anja / Kestner, Roxane Isabelle / Jencio, Lara / Schäufele, Tim J / Vutukuri, Rajkumar / Pfeilschifter, Waltraud / Scholich, Klaus

    Cells

    2022  Volume 11, Issue 10

    Abstract: Ischemic stroke is a highly prevalent vascular disease leading to oxygen- and glucose deprivation in the brain. In response, ischemia-induced neovascularization occurs, which is supported by circulating ... ...

    Abstract Ischemic stroke is a highly prevalent vascular disease leading to oxygen- and glucose deprivation in the brain. In response, ischemia-induced neovascularization occurs, which is supported by circulating CD34
    MeSH term(s) Animals ; Brain Ischemia/pathology ; Cicatrix/pathology ; Endothelial Cells/pathology ; Infarction, Middle Cerebral Artery/pathology ; Mice ; Neovascularization, Pathologic/pathology ; Stroke/complications ; Stroke/pathology
    Language English
    Publishing date 2022-05-17
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells11101659
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Eosinophil-derived IL-4 is necessary to establish the inflammatory structure in innate inflammation.

    Kolbinger, Anja / Schäufele, Tim J / Steigerwald, Hanna / Friedel, Joschua / Pierre, Sandra / Geisslinger, Gerd / Scholich, Klaus

    EMBO molecular medicine

    2022  Volume 15, Issue 2, Page(s) e16796

    Abstract: Pathogen-induced inflammation comprises pro- and anti-inflammatory processes, which ensure pathogen removal and containment of the proinflammatory activities. Here, we aimed to identify the development of inflammatory microenvironments and their ... ...

    Abstract Pathogen-induced inflammation comprises pro- and anti-inflammatory processes, which ensure pathogen removal and containment of the proinflammatory activities. Here, we aimed to identify the development of inflammatory microenvironments and their maintenance throughout the course of a toll-like receptor 2-mediated paw inflammation. Within 24 h after pathogen-injection, the immune cells were organized in three zones, which comprised a pathogen-containing "core-region", a bordering proinflammatory (PI)-region and an outer anti-inflammatory (AI)-region. Eosinophils were present in all three inflammatory regions and adapted their cytokine profile according to their localization. Eosinophil depletion reduced IL-4 levels and increased edema formation as well as mechanical and thermal hypersensitivities during resolution of inflammation. Also, in the absence of eosinophils PI- and AI-regions could not be determined anymore, neutrophil numbers increased, and efferocytosis as well as M2-macrophage polarization were reduced. IL-4 administration restored in eosinophil-depleted mice PI- and AI-regions, normalized neutrophil numbers, efferocytosis, M2-macrophage polarization as well as resolution of zymosan-induced hypersensitivity. In conclusion, IL-4-expressing eosinophils support the resolution of inflammation by enabling the development of an anti-inflammatory framework, which encloses proinflammatory regions.
    MeSH term(s) Animals ; Mice ; Anti-Inflammatory Agents ; Eosinophils ; Inflammation ; Interleukin-4 ; Neutrophils
    Chemical Substances Anti-Inflammatory Agents ; Interleukin-4 (207137-56-2) ; Il4 protein, mouse
    Language English
    Publishing date 2022-12-21
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2467145-9
    ISSN 1757-4684 ; 1757-4676
    ISSN (online) 1757-4684
    ISSN 1757-4676
    DOI 10.15252/emmm.202216796
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6784: Show issues Location:
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  4. Article ; Online: T-Cell-Specific CerS4 Depletion Prolonged Inflammation and Enhanced Tumor Burden in the AOM/DSS-Induced CAC Model.

    El-Hindi, Khadija / Brachtendorf, Sebastian / Hartel, Jennifer Christina / Oertel, Stephanie / Birod, Kerstin / Merz, Nadine / Trautmann, Sandra / Thomas, Dominique / Weigert, Andreas / Schäufele, Tim J / Scholich, Klaus / Schiffmann, Susanne / Ulshöfer, Thomas / Utermöhlen, Olaf / Grösch, Sabine

    International journal of molecular sciences

    2022  Volume 23, Issue 3

    Abstract: To better understand the role of sphingolipids in the multifactorial process of inflammatory bowel disease (IBD), we elucidated the role of CerS4 in colitis and colitis-associated cancer (CAC). For this, we utilized the azoxymethane/dextran sodium ... ...

    Abstract To better understand the role of sphingolipids in the multifactorial process of inflammatory bowel disease (IBD), we elucidated the role of CerS4 in colitis and colitis-associated cancer (CAC). For this, we utilized the azoxymethane/dextran sodium sulphate (AOM/DSS)-induced colitis model in global CerS4 knockout (CerS4 KO), intestinal epithelial (CerS4 Vil/Cre), or T-cell restricted knockout (CerS4 LCK/Cre) mice. CerS4 KO mice were highly sensitive to the toxic effect of AOM/DSS, leading to a high mortality rate. CerS4 Vil/Cre mice had smaller tumors than WT mice. In contrast, CerS4 LCK/Cre mice frequently suffered from pancolitis and developed more colon tumors. In vitro, CerS4-depleted CD8+ T-cells isolated from the thymi of CerS4 LCK/Cre mice showed impaired proliferation and prolonged cytokine production after stimulation in comparison with T-cells from WT mice. Depletion of CerS4 in human Jurkat T-cells led to a constitutively activated T-cell receptor and NF-κB signaling pathway. In conclusion, the deficiency of CerS4 in T-cells led to an enduring active status of these cells and prevents the resolution of inflammation, leading to a higher tumor burden in the CAC mouse model. In contrast, CerS4 deficiency in epithelial cells resulted in smaller colon tumors and seemed to be beneficial. The higher tumor incidence in CerS4 LCK/Cre mice and the toxic effect of AOM/DSS in CerS4 KO mice exhibited the importance of CerS4 in other tissues and revealed the complexity of general targeting CerS4.
    MeSH term(s) Animals ; Azoxymethane/adverse effects ; Colitis-Associated Neoplasms/chemically induced ; Colitis-Associated Neoplasms/genetics ; Colitis-Associated Neoplasms/immunology ; Colitis-Associated Neoplasms/pathology ; Colonic Neoplasms/chemically induced ; Colonic Neoplasms/genetics ; Colonic Neoplasms/immunology ; Colonic Neoplasms/pathology ; Dextran Sulfate/adverse effects ; Disease Models, Animal ; Gene Expression Regulation, Neoplastic ; Humans ; Jurkat Cells ; Mice ; Mice, Knockout ; NF-kappa B/metabolism ; Organ Specificity ; Receptors, Antigen, T-Cell/metabolism ; Signal Transduction ; Sphingosine N-Acyltransferase/genetics ; T-Lymphocytes/metabolism ; Tumor Burden
    Chemical Substances NF-kappa B ; Receptors, Antigen, T-Cell ; Dextran Sulfate (9042-14-2) ; CERS4 protein, mouse (EC 2.3.1.24) ; Sphingosine N-Acyltransferase (EC 2.3.1.24) ; Azoxymethane (MO0N1J0SEN)
    Language English
    Publishing date 2022-02-07
    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/ijms23031866
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: A bicistronic vector backbone for rapid seamless cloning and chimerization of αβT-cell receptor sequences.

    Kropp, Korbinian N / Schäufele, Tim J / Fatho, Martina / Volkmar, Michael / Conradi, Roland / Theobald, Matthias / Wölfel, Thomas / Wölfel, Catherine

    PloS one

    2020  Volume 15, Issue 9, Page(s) e0238875

    Abstract: To facilitate preclinical testing of T-cell receptors (TCRs) derived from tumor-reactive T-cell clones it is necessary to develop convenient and rapid cloning strategies for the generation of TCR expression constructs. Herein, we describe a pDONR™221 ... ...

    Abstract To facilitate preclinical testing of T-cell receptors (TCRs) derived from tumor-reactive T-cell clones it is necessary to develop convenient and rapid cloning strategies for the generation of TCR expression constructs. Herein, we describe a pDONR™221 vector backbone allowing to generate Gateway™ compatible entry clones encoding optimized bicistronic αβTCR constructs. It harbors P2A-linked TCR constant regions and head-to-head-oriented recognition sites of the Type IIS restriction enzymes BsmBI and BsaI for seamless cloning of the TCRα and TCRβ V(D)J regions, respectively. Additional well-established TCR optimizations were incorporated to enhance TCR functionality. This included replacing of the human αβTCR constant regions with their codon-optimized murine counterparts for chimerization, addition of a second interchain disulfide bond and arrangement of the TCR chains in the order β-P2A-α. We exemplified the utility of our vector backbone by cloning and functional testing of three melanoma-reactive TCRs in primary human T cells.
    MeSH term(s) Animals ; COS Cells ; Cell Line ; Chlorocebus aethiops ; Cloning, Molecular/methods ; Coculture Techniques ; Genetic Vectors/genetics ; HEK293 Cells ; Humans ; Receptors, Antigen, T-Cell, alpha-beta/genetics ; Retroviridae/genetics ; T-Lymphocytes/cytology ; T-Lymphocytes/immunology ; T-Lymphocytes/virology ; Transduction, Genetic ; V(D)J Recombination
    Chemical Substances Receptors, Antigen, T-Cell, alpha-beta
    Language English
    Publishing date 2020-09-09
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 1932-6203
    ISSN (online) 1932-6203
    DOI 10.1371/journal.pone.0238875
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Bacterial and Fungal Toll-Like Receptor Activation Elicits Type I IFN Responses in Mast Cells.

    Kornstädt, Lisa / Pierre, Sandra / Weigert, Andreas / Ebersberger, Stefanie / Schäufele, Tim J / Kolbinger, Anja / Schmid, Tobias / Cohnen, Jennifer / Thomas, Dominique / Ferreirós, Nerea / Brüne, Bernhard / Ebersberger, Ingo / Scholich, Klaus

    Frontiers in immunology

    2021  Volume 11, Page(s) 607048

    Abstract: Next to their role in IgE-mediated allergic diseases and in promoting inflammation, mast cells also have antiinflammatory functions. They release pro- as well as antiinflammatory mediators, depending on the biological setting. Here we aimed to better ... ...

    Abstract Next to their role in IgE-mediated allergic diseases and in promoting inflammation, mast cells also have antiinflammatory functions. They release pro- as well as antiinflammatory mediators, depending on the biological setting. Here we aimed to better understand the role of mast cells during the resolution phase of a local inflammation induced with the Toll-like receptor (TLR)-2 agonist zymosan. Multiple sequential immunohistology combined with a statistical neighborhood analysis showed that mast cells are located in a predominantly antiinflammatory microenvironment during resolution of inflammation and that mast cell-deficiency causes decreased efferocytosis in the resolution phase. Accordingly, FACS analysis showed decreased phagocytosis of zymosan and neutrophils by macrophages in mast cell-deficient mice. mRNA sequencing using zymosan-induced bone marrow-derived mast cells (BMMC) revealed a strong type I interferon (IFN) response, which is known to enhance phagocytosis by macrophages. Both, zymosan and lipopolysaccharides (LPS) induced IFN-β synthesis in BMMCs in similar amounts as in bone marrow derived macrophages. IFN-β was expressed by mast cells in paws from naïve mice and during zymosan-induced inflammation. As described for macrophages the release of type I IFNs from mast cells depended on TLR internalization and endosome acidification. In conclusion, mast cells are able to produce several mediators including IFN-β, which are alone or in combination with each other able to regulate the phagocytotic activity of macrophages during resolution of inflammation.
    MeSH term(s) Animals ; Cells, Cultured ; Chymases/genetics ; Chymases/metabolism ; Diphtheria Toxin/genetics ; Diphtheria Toxin/metabolism ; Disease Models, Animal ; Female ; Inflammation/chemically induced ; Inflammation/genetics ; Inflammation/immunology ; Inflammation/metabolism ; Interferon Type I/genetics ; Interferon Type I/metabolism ; Lipopolysaccharides/pharmacology ; Macrophages/immunology ; Macrophages/metabolism ; Male ; Mast Cells/drug effects ; Mast Cells/immunology ; Mast Cells/metabolism ; Mice, Inbred C57BL ; Mice, Transgenic ; Neutrophils/immunology ; Neutrophils/metabolism ; Phagocytosis ; Signal Transduction ; Toll-Like Receptors/agonists ; Toll-Like Receptors/metabolism ; Zymosan ; Mice
    Chemical Substances Diphtheria Toxin ; Interferon Type I ; Lipopolysaccharides ; Toll-Like Receptors ; Zymosan (9010-72-4) ; Cma1 protein, mouse (EC 3.4.21.-) ; Chymases (EC 3.4.21.39)
    Language English
    Publishing date 2021-02-12
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2020.607048
    Database MEDical Literature Analysis and Retrieval System OnLINE

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