Library

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Electronic Resource
    Electronic Resource
    Differences in LPS-Induced Activation of Bronchial Epithelial Cells (BEAS-2B) and Type II-Like Pneumocytes (A-549) (2002)
    Oxford, UK : Blackwell Science Ltd
    Scandinavian journal of immunology 56 (2002), S. 0 
    Details
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Lipopolysaccharide (LPS) as a major component of the outer membrane of gram-negative bacteria stimulates various cells to initiate a signalling cascade which ultimately leads to cell activation and expression of immunoregulatory or inflammatory cytokines. The human respiratory epithelium is an important environmental interface, but differences in LPS-induced cell activation between bronchial and alveolar epithelial cells have not yet been investigated in detail. First, the expression of Toll-like receptors (TLRs), as pattern-recognition receptors, was investigated for the bronchial epithelial cells and type II-like pneumocytes, demonstrating that they fulfil the prerequisites for LPS signalling. Thereafter, the effects of LPS, soluble CD14 (sCD14) and LPS-binding protein (LBP) on the release of interleukin-6 (IL-6) and IL-8 were studied. In the presence of LPS, sCD14 induced a significant and concentration-dependent cytokine release in type II-like pneumocytes, whereas the response of bronchial epithelial cells to sCD14 stimulation was low, implicating sCD14-independent activation mechanisms. Furthermore, LBP revealed inhibitory effects on the activation of alveolar epithelial cells, which may represent a novel local defence mechanism during gram-negative infection. We conclude that distinct pathways exist for LPS-induced activation of bronchial and alveolar epithelial cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-3083.2002.01137.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Interferon (IFN)-γ is a main mediator of keratinocyte (HaCaT) apoptosis and contributes to autocrine IFN-γ and tumour necrosis factor-α production (2005)
    Oxford, UK : Blackwell Science Ltd
    British journal of dermatology 152 (2005), S. 0 
    Details
    ISSN: 1365-2133
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background  Apoptosis of keratinocytes or intestinal epithelial cells is an important pathophysiological mechanism of organ damage during acute graft-versus-host disease.Objectives  To analyse in detail the mediators and their mutual interaction leading to keratinocyte apoptosis.Methods  Experiments were performed using a keratinocyte cell line (HaCaT) and human skin explant cultures.Results  Supernatants (SN) of major histocompatibility complex nonmatched mixed lymphocyte cultures (MLCs) induced apoptosis in HaCaT cells and also in keratinocytes from skin biopsies. Although both interferon (IFN)-γ and Fas ligand (FasL) were detected in MLC-SN by enzyme-linked immunosorbent assay, the apoptosis-inducing capacity could be fully abrogated by neutralization of IFN-γ, but not by neutralization of FasL. Recombinant (r) IFN-γ induced HaCaT keratinocyte apoptosis in a dose- and time-dependent manner. Induction of HaCaT apoptosis by rFasL alone was induced only at higher doses than present in MLC-SN, but apoptosis was dramatically enhanced in the presence of rIFN-γ. Further synergistic effects with IFN-γ in the induction of apoptosis were also observed with agonistic antitumour necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) receptor 2 antibody, soluble TRAIL and TNF-α. However, in contrast to FasL and TRAIL, TNF-α alone did not induce HaCaT apoptosis. Interleukin-1β and lipopolysaccharide did not enhance the apoptosis-inducing effect of IFN-γ. Beside its apoptosis-inducing capacity in HaCaT cells, rIFN-γ also induced autocrine IFN-γ production, and combined treatment with IFN-γ and TNF-α induced autocrine TNF-α production. Neutralization of autocrine IFN-γ protected HaCaT cells from apoptosis.Conclusions  Taken together, our data suggest a central role for IFN-γ in HaCaT keratinocyte apoptosis but also show the importance of co-acting mediators such as TNF-α, TRAIL and FasL, which potentiate the effect of paracrine and autocrine IFN-γ and TNF-α release.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2133.2005.06508.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Protein Kinase C Activation is Involved in Ultraviolet B Irradiation-Induced Endothelial Cell ICAM-1 Up-Regulation and Lymphocyte–Endothelium Interaction In Vitro (1996)
    Oxford, U.K. and Cambridge, USA : Blackwell Science Ltd
    Scandinavian journal of immunology 44 (1996), S. 0 
    Details
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Lymphocyte–endothelium interactions are pivotal steps in mediating inflammatory responses. The authors have analysed the influence of ultraviolet B (UVB) irradiation on intercellular adhesion molecule (ICAM)-1 expression on cells of the human microvascular endothelial cell line (HMEC)-1 and the intracellular signalling pathways involved. Flow cytometry revealed dose-dependent ICAM-1 up-regulation with maximum induced expression 24 h after sublethal UVB irradiation of 10 mJ/cm2. While anti-tumour necrosis factor (TNF)-α antibodies or recombinant human interleukin (IL)-10 did not influence this response, anti-interferon (IFN)-γ antibodies blocked the UVB-induced ICAM-1 up-regulation. Significant induction of intracellular/membrane-bound IFN-γ was measured as early as 6 h post-UVB. Since previous work has shown a differential role of protein kinase C (PKC) in cytokine induced ICAM-1 expression, the effect of a selective  bisindolylmaleimide-derived PKC-inhibitor (GF109203X) was studied. Ultraviolet B-induced ICAM-1 up-regulation was effectively blocked by the PKC-inhibitor, whereas a PKA-inhibitor was ineffective. Moreover, immunofluorescence analysis showed a radiation-induced membrane translocation of PKC-α, indicative of enzyme activation, in HMEC-1 cells already 30 min post-UVB. The functional relevance of the UVB-induced ICAM-1 expression and involvement of PKC in this process was demonstrated in an adhesion assay with peripheral blood mononuclear cells. In conclusion, UVB-induced ICAM-1 expression on human endothelial cells involves PKC-dependent pathways and can be prevented by a PKC-inhibitor. The use of PKC-inhibitors as additive modulators in immune reactions may bear clinical potential. The mechanisms of IFN-γ induction in endothelial cells by UVB deserve further investigation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-3083.1996.d01-324.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    Differential Role of Protein Kinase C in Cytokine Induced Lymphocyte-Endothelium Interaction In Vitro (1994)
    Oxford, UK : Blackwell Publishing Ltd
    Scandinavian journal of immunology 40 (1994), S. 0 
    Details
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: In the present study we investigated the influence of the PKC-inhibitor GF109203X on cytokine- and endotoxin-induced expression of intercellular adhesion molecule 1 (ICAM-1) and on the adhesion of lymphocytes to cytokine-activated endothelial cells. We found that tumour necrosis factor alpha (TNF-α)- and lipopolysaccharide (LPS)-induced ICAM-I expression on a human endothelium-derived cell line (EA. hy926) were unaffected by the PKC-inhibitor and thus appeared to be independent of PKC activation. In contrast, GF109203X significantly reduced ICAM-1 expression induced by interferon-γ (IFN-γ) and interleukin-1 (IL-1). The functional relevance of these findings was evaluated in an adhesion assay using human umbilical vein endothelial cells (HUVEC) and peripheral blood mono-nuclear cells (PBMC). In fact, the IFN-γ- and IL-1-induced adhesion of PBMC to cytokine treated HUVEC could be down-regulated by the PKC-inhibitor, whereas TNF-α and LPS-mediated adhesion was not affected. Additionally, the IL-1-driven ICAM-1 expression on HUVEC as well as the IL-I induced adhesion of PBMC to HUVEC was found to be TNF-dependent, as both effects could be inhibited by an anti-TNF-α monoclonal antibody (MoAb) (MAK195). Based on these data on differential regulation of cytokine-induced lymphocyte-indothelium interactions our study supports the use of PKC-inhibitors as additive modulators in cytokine related pathophysiological conditions.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-3083.1994.tb03480.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...