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  1. AU="Szymanski, Kolja"
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  1. Book ; Online ; Thesis: Streptococcus pneumoniae und Influenza A Virus induzierte Immunantwort in kultiviertem, humanem Lungengewebe und Zellkulturen

    Szymanski, Kolja

    2014  

    Title variant Streptococcus pneumoniae and Influenza A virus induced immune response in cultivated, human lung tissue and cell cultures
    Author's details Kolja Szymanski
    Language German
    Size Online-Ressource
    Publisher Medizinische Fakultät Charité - Universitätsmedizin Berlin
    Publishing place Berlin
    Document type Book ; Online ; Thesis
    Thesis / German Habilitation thesis Berlin, Medizinische Fakultät Charité - Universitätsmedizin Berlin, Diss., 2014
    Database Former special subject collection: coastal and deep sea fishing

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  2. Book ; Online ; Thesis: Streptococcus pneumoniae und Influenza A Virus induzierte Immunantwort in kultiviertem, humanem Lungengewebe und Zellkulturen

    Szymanski, Kolja [Verfasser]

    2014  

    Author's details Kolja Szymanski
    Keywords Medizin, Gesundheit ; Medicine, Health
    Subject code sg610
    Language German
    Publisher Medizinische Fakultät Charité - Universitätsmedizin Berlin
    Publishing place Berlin
    Document type Book ; Online ; Thesis
    Database Digital theses on the web

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  3. Article ; Online: Streptococcus pneumoniae induces human β-defensin-2 and -3 in human lung epithelium.

    Scharf, Stefanie / Zahlten, Janine / Szymanski, Kolja / Hippenstiel, Stefan / Suttorp, Norbert / N'Guessan, Philippe Dje

    Experimental lung research

    2012  Volume 38, Issue 2, Page(s) 100–110

    Abstract: Streptococcus pneumoniae is an important causative agent of pneumonia in humans. Pulmonary epithelial surfaces constitutes not only a mechanical barrier against invading pathogens but also essentially contribute to innate immunity by producing ... ...

    Abstract Streptococcus pneumoniae is an important causative agent of pneumonia in humans. Pulmonary epithelial surfaces constitutes not only a mechanical barrier against invading pathogens but also essentially contribute to innate immunity by producing antimicrobial peptides such as human β-defensin-2 (hBD-2) and -3 (hBD-3). In this study the authors demonstrated that pneumococci induced hBD-2 and hBD-3 expression in human pulmonary epithelial cells. Further analysis indicated an essential role of Toll-like receptor 2 (TLR2) for the expression of both peptides in infected pulmonary epithelial cells. Whereas the hBD-2 release was controlled by the phosphoinositide 3-kinase (PI3K) and the transcription factor nuclear factor kappa B (NF-κB), hBD-3 was triggered via the c-Jun N-terminal kinase (JNK)-activator protein 1 (AP-1) pathway. Additionally, the authors showed that exogenous hBD-2 as well as hBD-3 elicited a strong antimicrobial effect on S. pneumoniae. Thus, differential regulation of the expression of hBD-2 and hBD-3 might play an important role in pneumococci pneumonia.
    MeSH term(s) Alveolar Epithelial Cells/immunology ; Alveolar Epithelial Cells/metabolism ; Alveolar Epithelial Cells/microbiology ; Humans ; Immunity, Innate ; Lung/immunology ; Lung/metabolism ; Lung/microbiology ; NF-kappa B/metabolism ; Phosphatidylinositol 3-Kinase/metabolism ; Proto-Oncogene Proteins c-jun/metabolism ; Streptococcus pneumoniae/immunology ; Streptococcus pneumoniae/pathogenicity ; Toll-Like Receptor 2/metabolism ; Transcription Factor AP-1/metabolism ; beta-Defensins/biosynthesis
    Chemical Substances DEFB103A protein, human ; DEFB4A protein, human ; NF-kappa B ; Proto-Oncogene Proteins c-jun ; TLR2 protein, human ; Toll-Like Receptor 2 ; Transcription Factor AP-1 ; beta-Defensins ; Phosphatidylinositol 3-Kinase (EC 2.7.1.137)
    Language English
    Publishing date 2012-01-18
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 603791-4
    ISSN 1521-0499 ; 0190-2148
    ISSN (online) 1521-0499
    ISSN 0190-2148
    DOI 10.3109/01902148.2011.652802
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 1568: Show issues Location:
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  4. Article ; Online: Sphingosine Kinase 1 Regulates Inflammation and Contributes to Acute Lung Injury in Pneumococcal Pneumonia via the Sphingosine-1-Phosphate Receptor 2.

    Gutbier, Birgitt / Schönrock, Stefanie M / Ehrler, Carolin / Haberberger, Rainer / Dietert, Kristina / Gruber, Achim D / Kummer, Wolfgang / Michalick, Laura / Kuebler, Wolfgang M / Hocke, Andreas C / Szymanski, Kolja / Letsiou, Eleftheria / Lüth, Anja / Schumacher, Fabian / Kleuser, Burkhard / Mitchell, Timothy J / Bertrams, Wilhelm / Schmeck, Bernd / Treue, Denise /
    Klauschen, Frederick / Bauer, Torsten T / Tönnies, Mario / Weissmann, Norbert / Hippenstiel, Stefan / Suttorp, Norbert / Witzenrath, Martin

    Critical care medicine

    2018  Volume 46, Issue 3, Page(s) e258–e267

    Abstract: Objectives: Severe pneumonia may evoke acute lung injury, and sphingosine-1-phosphate is involved in the regulation of vascular permeability and immune responses. However, the role of sphingosine-1-phosphate and the sphingosine-1-phosphate producing ... ...

    Abstract Objectives: Severe pneumonia may evoke acute lung injury, and sphingosine-1-phosphate is involved in the regulation of vascular permeability and immune responses. However, the role of sphingosine-1-phosphate and the sphingosine-1-phosphate producing sphingosine kinase 1 in pneumonia remains elusive. We examined the role of the sphingosine-1-phosphate system in regulating pulmonary vascular barrier function in bacterial pneumonia.
    Design: Controlled, in vitro, ex vivo, and in vivo laboratory study.
    Subjects: Female wild-type and SphK1-deficient mice, 8-10 weeks old. Human postmortem lung tissue, human blood-derived macrophages, and pulmonary microvascular endothelial cells.
    Interventions: Wild-type and SphK1-deficient mice were infected with Streptococcus pneumoniae. Pulmonary sphingosine-1-phosphate levels, messenger RNA expression, and permeability as well as lung morphology were analyzed. Human blood-derived macrophages and human pulmonary microvascular endothelial cells were infected with S. pneumoniae. Transcellular electrical resistance of human pulmonary microvascular endothelial cell monolayers was examined. Further, permeability of murine isolated perfused lungs was determined following exposition to sphingosine-1-phosphate and pneumolysin.
    Measurements and main results: Following S. pneumoniae infection, murine pulmonary sphingosine-1-phosphate levels and sphingosine kinase 1 and sphingosine-1-phosphate receptor 2 expression were increased. Pneumonia-induced lung hyperpermeability was reduced in SphK1 mice compared with wild-type mice. Expression of sphingosine kinase 1 in macrophages recruited to inflamed lung areas in pneumonia was observed in murine and human lungs. S. pneumoniae induced the sphingosine kinase 1/sphingosine-1-phosphate system in blood-derived macrophages and enhanced sphingosine-1-phosphate receptor 2 expression in human pulmonary microvascular endothelial cell in vitro. In isolated mouse lungs, pneumolysin-induced hyperpermeability was dose dependently and synergistically increased by sphingosine-1-phosphate. This sphingosine-1-phosphate-induced increase was reduced by inhibition of sphingosine-1-phosphate receptor 2 or its downstream effector Rho-kinase.
    Conclusions: Our data suggest that targeting the sphingosine kinase 1-/sphingosine-1-phosphate-/sphingosine-1-phosphate receptor 2-signaling pathway in the lung may provide a novel therapeutic perspective in pneumococcal pneumonia for prevention of acute lung injury.
    MeSH term(s) Acute Lung Injury/enzymology ; Acute Lung Injury/etiology ; Acute Lung Injury/metabolism ; Animals ; Female ; Humans ; Inflammation/enzymology ; Inflammation/metabolism ; Mice ; Mice, Inbred C57BL ; Phosphotransferases (Alcohol Group Acceptor)/metabolism ; Pneumonia, Pneumococcal/complications ; Pneumonia, Pneumococcal/enzymology ; Pneumonia, Pneumococcal/metabolism ; Receptors, Lysosphingolipid/metabolism ; Streptococcus pneumoniae
    Chemical Substances Receptors, Lysosphingolipid ; S1PR2 protein, human ; sphingosine-1-phosphate receptor-2, mouse ; Phosphotransferases (Alcohol Group Acceptor) (EC 2.7.1.-) ; sphingosine kinase (EC 2.7.1.-)
    Language English
    Publishing date 2018-01-23
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 197890-1
    ISSN 1530-0293 ; 0090-3493
    ISSN (online) 1530-0293
    ISSN 0090-3493
    DOI 10.1097/CCM.0000000000002916
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1261: Show issues Location:
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  5. Article ; Online: Influenza A viruses target type II pneumocytes in the human lung.

    Weinheimer, Viola K / Becher, Anne / Tönnies, Mario / Holland, Gudrun / Knepper, Jessica / Bauer, Torsten T / Schneider, Paul / Neudecker, Jens / Rückert, Jens C / Szymanski, Kolja / Temmesfeld-Wollbrueck, Bettina / Gruber, Achim D / Bannert, Norbert / Suttorp, Norbert / Hippenstiel, Stefan / Wolff, Thorsten / Hocke, Andreas C

    The Journal of infectious diseases

    2012  Volume 206, Issue 11, Page(s) 1685–1694

    Abstract: Background: Highly pathogenic avian H5N1 influenza viruses preferentially infect alveolar type II pneumocytes in human lung. However, it is unknown whether this cellular tropism contributes to high viral virulence because the primary target cells of ... ...

    Abstract Background: Highly pathogenic avian H5N1 influenza viruses preferentially infect alveolar type II pneumocytes in human lung. However, it is unknown whether this cellular tropism contributes to high viral virulence because the primary target cells of other influenza viruses have not been systematically studied.
    Methods: We provide the first comparison of the replication, tropism, and cytokine induction of human, highly pathogenic avian influenza A virus subtype H5N1 and other animal influenza A viruses in primary human lung organ cultures.
    Results: Subytpe H5N1 and human-adapted subtype H1N1 and H3N2 viruses replicated efficiently in the lung tissue, whereas classic swine and low-pathogenicity avian viruses propagated only poorly. Nevertheless, all viruses examined were detected almost exclusively in type II pneumocytes, with a minor involvement of alveolar macrophages. Infection with avian viruses that have a low and high pathogenicity provoked a pronounced induction of cytokines and chemokines, while human and pandemic H1N1-2009 viruses triggered only weak responses.
    Conclusions: These findings show that differences in the pathogenic potential of influenza A viruses in the human lung cannot be attributed to a distinct cellular tropism. Rather, high or low viral pathogenicity is associated with a strain-specific capacity to productively replicate in type II pneumocytes and to cope with the induced cytokine response.
    MeSH term(s) Alveolar Epithelial Cells/classification ; Alveolar Epithelial Cells/virology ; Cytokines/genetics ; Cytokines/metabolism ; Gene Expression Regulation/physiology ; Humans ; Influenza A virus/classification ; Influenza A virus/pathogenicity ; Influenza A virus/physiology ; Influenza, Human/virology ; Lung/cytology ; Macrophages, Alveolar/virology ; Tissue Culture Techniques ; Viral Tropism/physiology ; Virulence ; Virus Replication/physiology
    Chemical Substances Cytokines
    Keywords covid19
    Language English
    Publishing date 2012-07-24
    Publishing country United States
    Document type Journal Article ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 3019-3
    ISSN 1537-6613 ; 0022-1899
    ISSN (online) 1537-6613
    ISSN 0022-1899
    DOI 10.1093/infdis/jis455
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    Uh II Zs.50: Show issues Location:
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    Zs.MO 445: Show issues

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  6. Article ; Online: Streptococcus pneumoniae-induced regulation of cyclooxygenase-2 in human lung tissue.

    Szymanski, Kolja V / Toennies, Mario / Becher, Anne / Fatykhova, Diana / N'Guessan, Philippe D / Gutbier, Birgitt / Klauschen, Frederick / Neuschaefer-Rube, Frank / Schneider, Paul / Rueckert, Jens / Neudecker, Jens / Bauer, Torsten T / Dalhoff, Klaus / Drömann, Daniel / Gruber, Achim D / Kershaw, Olivia / Temmesfeld-Wollbrueck, Bettina / Suttorp, Norbert / Hippenstiel, Stefan /
    Hocke, Andreas C

    The European respiratory journal

    2012  Volume 40, Issue 6, Page(s) 1458–1467

    Abstract: The majority of cases of community-acquired pneumonia are caused by Streptococcus pneumoniae and most studies on pneumococcal host interaction are based on cell culture or animal experiments. Thus, little is known about infections in human lung tissue. ... ...

    Abstract The majority of cases of community-acquired pneumonia are caused by Streptococcus pneumoniae and most studies on pneumococcal host interaction are based on cell culture or animal experiments. Thus, little is known about infections in human lung tissue. Cyclooxygenase-2 and its metabolites play an important regulatory role in lung inflammation. Therefore, we established a pneumococcal infection model on human lung tissue demonstrating mitogen-activated protein kinase (MAPK)-dependent induction of cyclooxygenase-2 and its related metabolites. In addition to alveolar macrophages and the vascular endothelium, cyclooxygenase-2 was upregulated in alveolar type II but not type I epithelial cells, which was confirmed in lungs of patients suffering from acute pneumonia. Moreover, we demonstrated the expression profile of all four E prostanoid receptors at the mRNA level and showed functionality of the E prostanoid(4) receptor by cyclic adenosine monophosphate production. Additionally, in comparison to previous studies, cyclooxygenase-2/prostaglandin E(2) related pro- and anti-inflammatory mediator regulation was partly confirmed in human lung tissue after pneumococcal infection. Overall, cell type-specific and MAPK-dependent cyclooxygenase-2 expression and prostaglandin E(2) formation in human lung tissue may play an important role in the early phase of pneumococcal infections.
    MeSH term(s) Colony-Forming Units Assay ; Cyclooxygenase 2/metabolism ; Dinoprostone/metabolism ; Epithelial Cells/microbiology ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Gene Expression Profiling ; Gene Expression Regulation, Bacterial ; Gene Expression Regulation, Enzymologic ; Humans ; Immunohistochemistry/methods ; Inflammation ; Lung/enzymology ; Lung/microbiology ; MAP Kinase Signaling System ; Microscopy, Fluorescence/methods ; Pneumococcal Infections/enzymology ; Pneumococcal Infections/microbiology ; Prostaglandins/metabolism ; Pulmonary Alveoli/microbiology ; Streptococcus pneumoniae/metabolism
    Chemical Substances Prostaglandins ; Cyclooxygenase 2 (EC 1.14.99.1) ; Extracellular Signal-Regulated MAP Kinases (EC 2.7.11.24) ; Dinoprostone (K7Q1JQR04M)
    Language English
    Publishing date 2012-12
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 639359-7
    ISSN 1399-3003 ; 0903-1936
    ISSN (online) 1399-3003
    ISSN 0903-1936
    DOI 10.1183/09031936.00186911
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 2322: Show issues Location:
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    Zs.MO 292: Show issues

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