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  1. AU="van Sterkenburg, M A J A"
  2. AU="Sayed Masoud Hosseini"
  3. AU="Pathania, Deepak"
  4. AU=Xu Yuzhong AU=Xu Yuzhong
  5. AU="Mehmood, Huzaifa"
  6. AU="Etcheverry, Amandine"
  7. AU="Sein, Andrea M"
  8. AU="Vo, Thi-Phi-Giao"
  9. AU="Allan, Alasdair"
  10. AU="Thurlow, Lance R"
  11. AU="Lum, Krystal"
  12. AU="Wilms, Miriam"
  13. AU="Russell, Michael H"
  14. AU="Bedoya-Arias, Hugo A"
  15. AU="Hijri, Mohamed"
  16. AU="Priscilla Gates"
  17. AU="Reiber, Matthew"
  18. AU="Bauer-Rowe, Khristian E"
  19. AU="Tanner, Martin E"
  20. AU="Creech, Gardner S"
  21. AU="José P. Oliveira-Filho"
  22. AU="Munt, Jennifer E"
  23. AU="Whiley, Phillip J"
  24. AU="V.Sudhir, "
  25. AU="Chatow, Lior"
  26. AU=Xue Zhe
  27. AU="Peter D. Yurchenco"
  28. AU="Várbíró, Gábor"
  29. AU="Sheleg, Dmitriy"
  30. AU="Panzirer, David"

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  1. Artikel ; Online: Interleukin 13 exposure enhances vitamin D-mediated expression of the human cathelicidin antimicrobial peptide 18/LL-37 in bronchial epithelial cells.

    Schrumpf, J A / van Sterkenburg, M A J A / Verhoosel, R M / Zuyderduyn, S / Hiemstra, P S

    Infection and immunity

    2012  Band 80, Heft 12, Seite(n) 4485–4494

    Abstract: Vitamin D is an important regulator of the expression of antimicrobial peptides, and vitamin D deficiency is associated with respiratory infections. Regulating expression of antimicrobial peptides, such as the human cathelicidin antimicrobial peptide 18 ( ...

    Abstract Vitamin D is an important regulator of the expression of antimicrobial peptides, and vitamin D deficiency is associated with respiratory infections. Regulating expression of antimicrobial peptides, such as the human cathelicidin antimicrobial peptide 18 (hCAP18)/LL-37, by vitamin D in bronchial epithelial cells requires local conversion of 25(OH)-vitamin D(3) (25D(3)) into its bioactive metabolite, 1,25(OH)(2)-vitamin D(3) (1,25D(3)), by CYP27B1. Low circulating vitamin D levels in childhood asthma are associated with more-severe exacerbations, which are often associated with infections. Atopic asthma is accompanied by Th2-driven inflammation mediated by cytokines such as interleukin 4 (IL-4) and IL-13, and the effect of these cytokines on vitamin D metabolism and hCAP18/LL-37 expression is unknown. Therefore, we investigated this with well-differentiated bronchial epithelial cells. To this end, cells were treated with IL-13 with and without 25D(3), and expression of hCAP18/LL-37, CYP27B1, the 1,25D(3)-inactivating enzyme CYP24A1, and vitamin D receptor was assessed by quantitative PCR. We show that IL-13 enhances the ability of 25D(3) to increase expression of hCAP18/LL-37 and CYP24A1. In addition, exposure to IL-13 resulted in increased CYP27B1 expression, whereas vitamin D receptor (VDR) expression was not significantly affected. The enhancing effect of IL-13 on 25D(3)-mediated expression of hCAP18/LL-37 was further confirmed using SDS-PAGE Western blotting and immunofluorescence staining. In conclusion, we demonstrate that IL-13 induces vitamin D-dependent hCAP18/LL-37 expression, most likely by increasing CYP27B1. These data suggest that Th2 cytokines regulate the vitamin D metabolic pathway in bronchial epithelial cells.
    Mesh-Begriff(e) Adjuvants, Immunologic/genetics ; Adjuvants, Immunologic/metabolism ; Antimicrobial Cationic Peptides ; Bronchi/cytology ; Bronchi/drug effects ; Bronchi/metabolism ; Cathelicidins/genetics ; Cathelicidins/metabolism ; Cells, Cultured ; Cholecalciferol/genetics ; Cholecalciferol/metabolism ; Cholecalciferol/pharmacology ; Epithelial Cells/drug effects ; Epithelial Cells/metabolism ; Humans ; Interleukin-13/genetics ; Interleukin-13/metabolism ; Interleukin-13/pharmacology ; Receptors, Calcitriol/genetics ; Receptors, Calcitriol/metabolism ; Up-Regulation/drug effects ; Vitamin D/analogs & derivatives ; Vitamin D/genetics ; Vitamin D/metabolism
    Chemische Substanzen Adjuvants, Immunologic ; Antimicrobial Cationic Peptides ; Cathelicidins ; Interleukin-13 ; Receptors, Calcitriol ; Vitamin D (1406-16-2) ; Cholecalciferol (1C6V77QF41) ; ropocamptide (3DD771JO2H)
    Sprache Englisch
    Erscheinungsdatum 2012-10-08
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 218698-6
    ISSN 1098-5522 ; 0019-9567
    ISSN (online) 1098-5522
    ISSN 0019-9567
    DOI 10.1128/IAI.06224-11
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel: Neutrophil defensins stimulate the release of cytokines by airway epithelial cells: modulation by dexamethasone.

    van Wetering, S / Mannesse-Lazeroms, S P G / van Sterkenburg, M A J A / Hiemstra, P S

    Inflammation research : official journal of the European Histamine Research Society ... [et al.

    2002  Band 51, Heft 1, Seite(n) 8–15

    Abstract: Objective and design: Neutrophils may contribute to recruiting other cells to sites of inflammation by generating chemotactic signals themselves, or by stimulating other cell types to release chemoattractants such as interleukin-8 (IL-8). Recently, we ... ...

    Abstract Objective and design: Neutrophils may contribute to recruiting other cells to sites of inflammation by generating chemotactic signals themselves, or by stimulating other cell types to release chemoattractants such as interleukin-8 (IL-8). Recently, we demonstrated that neutrophil-derived alpha-defensins are able to increase IL-8 expression in airway epithelial cells. In addition, it has previously been reported that neutrophil elastase-induced IL-8 synthesis was insensitive to inhibition by the glucocorticoid dexamethasone. The aim of the present study was to investigate the effect of defensins on the expression of various cytokines in cultured airway epithelial cells and to examine the effect of dexamethasone on defensin-induced cytokine synthesis in these cells.
    Methods: Cultures of A549 cells and primary bronchial epithelial cells (PBEC) were stimulated with defensins either alone or in the presence of dexamethasone. Supernatants were analyzed for IL-8, ENA-78, IL-6, MCP-1 and GM-CSF by ELISA. In addition, IL-8 and ENA-78 mRNA was detected by Northern blot analysis.
    Results: Defensins increased IL-8 expression, ENA-78, MCP-1 and GM-CSF release from A549 cells, whereas in PBEC only IL-8 and IL-6 were increased. Pre-treatment with dexamethasone significantly reduced defensin-induced IL-6, IL-8 and ENA-78 synthesis in airway epithelial cells. In addition, dexamethasone also reduced the neutrophil chemotactic activity in supernatants of these cells.
    Conclusions: The results from the present study indicate that defensins differentially induce cytokine secretion by A549 cells and PBEC. Glucocorticoids may interfere with the defensin-induced inflammatory process by reducing defensin-induced cytokine secretion in lung epithelial cells.
    Mesh-Begriff(e) Anti-Infective Agents/pharmacology ; Bronchi/metabolism ; Cells, Cultured ; Chemokine CXCL5 ; Chemokines, CXC ; Chemotaxis, Leukocyte/drug effects ; Defensins/pharmacology ; Dexamethasone/pharmacology ; Epithelial Cells/metabolism ; Humans ; Interleukin-8/analogs & derivatives ; Interleukin-8/biosynthesis ; Neutrophils/immunology
    Chemische Substanzen Anti-Infective Agents ; CXCL5 protein, human ; Chemokine CXCL5 ; Chemokines, CXC ; Defensins ; Interleukin-8 ; Dexamethasone (7S5I7G3JQL)
    Sprache Englisch
    Erscheinungsdatum 2002-01-17
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1221794-3
    ISSN 1420-908X ; 1023-3830
    ISSN (online) 1420-908X
    ISSN 1023-3830
    DOI 10.1007/pl00000282
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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    Verfügbar in ZB MED Köln/Königswinter

    Zs.A 675: Hefte anzeigen Standort:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

    Über subito bestellen

    Dieser Service ist kostenpflichtig (siehe Lieferbedingungen von subito). Bestellungen, die einen Artikel nebst Supplementary Material umfassen, werden grundsätzlich wie mehrfache Bestellungen bearbeitet. Gebühren fallen in diesen Fällen für jede einzelne Bestellung an.

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