GLORIA

GEOMAR Library Ocean Research Information Access

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
    Online Resource
    Online Resource
    Mechanismen der antibakteriellen Wirkung polykationischer Proteine aus Granulozyten (2002)
    Borstel
    Details Availability
    Description / Table of Contents: Sepsis, Gram-negative bacteria, outer membrane, antibacterial peptides/proteins, cathelicidines, lipopolysaccharide-binding protein (LBP)
    Type of Medium: Online Resource
    Pages: Online-Ressource (83., 11,9 Mb.)
    Edition: [Elektronische Ressource]
    Series Statement: Septischer Schock : molekulare Pathophysiologie und therapeutische Ansätze / Projektl.: Ulrich Seydel; Ernst Th. Rietschel; Teilprojekt A6
    URL: https://edocs.tib.eu/files/e01fb02/356559084.pdf
    URL: https://edocs.tib.eu/files/e01fb02/356559084l.pdf
    Language: German
    Note: Contract BMBF 01 KI 9851 A6. - Differences between the printed and electronic version of the document are possible. - nIndex p. 75 - 83. - Engl. title: Mechanisms of antibacterial actions of polycationic proteins of granulocytes , Also available as printed version , Systemvoraussetzungen: Acrobat Reader.
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    GEOMAR CATALOGUE
    Link to Library Catalog
    get availability status
  • 2
    Online Resource
    Online Resource
    Entwicklung und Erprobung neuer Instrumente zur Bildung von Verwertungs- und Transfernetzen innerhalb der Leibniz-Gemeinschaft: Gesamtstrategie, Koordination und Dokumentation der Maßnahme : Abschlussbericht ; Berichtszeitraum: 01.09.2007 - 28.02.2010 (2010)
    [Bonn]
    Details Availability
    Keywords: Forschungsbericht ; Wissenschaftsgemeinschaft Gottfried Wilhelm Leibniz ; Wissenschaftstransfer ; Technologietransfer ; Unternehmen
    Type of Medium: Online Resource
    Pages: Online-Ressource (59 S., 2,19 MB) , Ill., graph. Darst.
    URL: https://edocs.tib.eu/files/e01fb10/640164463.pdf
    URL: https://doi.org/10.2314/GBV:640164463
    URL: https://edocs.tib.eu/files/e01fb10/640164463l.pdf
    DOI: 10.2314/GBV:640164463
    Language: German
    Note: Förderkennzeichen BMBF 01SF0709 , Unterschiede zwischen dem gedruckten Dokument und der elektronischen Ressource können nicht ausgeschlossen werden. - Auch als gedr. Ausg. vorhanden , Systemvoraussetzungen: Acrobat reader. , Enth. als Anl. 8 die Broschüre "Verwertungsorientierte Netzwerke - Innovationsallianzen zwischen Wissenschaft und Wirtschaft"
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    GEOMAR CATALOGUE
    Link to Library Catalog
    get availability status
  • 3
    Electronic Resource
    Electronic Resource
    Diphosphoryl lipid A derived from the lipopolysaccharide (LPS) of Rhodobacter sphaeroides ATCC 17023 is a potent competitive LPS inhibitor in murine macrophage-like J774.1 cells (1994)
    Oxford, UK : Blackwell Publishing Ltd
    FEMS immunology and medical microbiology 9 (1994), S. 0 
    Details
    ISSN: 1574-695X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Notes: Abstract Pentaacyl diphosphoryllipid A derived from the nontoxic lipopolysaccharide (LPS) of Rhodobacter sphaeroides ATCC 17023 (RsDPLA) did not induce tumour necrosis factor-α nor interleukin-6 release in the murine macrophage-like cell line J774.1. However, it effectively inhibited the induction of these two cytokines by LPS of Salmonella minnesota Re mutant R595 (ReLPA) in a concentration-dependent manner. Maximal inhibition and half-maximal inhibition occured when the ReLPS to RsDPLA mass ratio was 1:30 and 1:1, respectively. A binding study was performed in the presence of serum to determine whether RsDPLA is competing with ReLPS for LPS binding sites on J774.1 cells. This assay allows the determination of LPS binding to J774.1 cells via a mechanism involving CD14, a receptor for complexes of LPS with LPS binding protein (LBP), and its possible inhibition. The results show that RsDPLA strongly inhibits the binding of 125I-labelled ReLPS to J774.1 cells. Maximal and one-half maximal inhibition of binding occured when the ReLPS to RsDPLA mass ratios were 1:2.5 and 1:0.5, respectively. It was found that the inhibition of binding by RsDPLA was much stronger than that by unlabelled ReLPS. These results suggest that RsDPLA is competing with ReLPS for CD14-dependent recognition of LPS on J774.1 cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1574-695X.1994.tb00499.x
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    The significance of the hydrophilic backbone and the hydrophobic fatty acid regions of lipid a for macrophage binding and cytokine induction (1994)
    Oxford, UK : Blackwell Publishing Ltd
    FEMS immunology and medical microbiology 8 (1994), S. 0 
    Details
    ISSN: 1574-695X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Notes: Abstract Natural partial structures of lipopolysaccharide (LPS) as well as synthetic analogues and derivatives of lipid A were compared with respect to inhibit the binding of 125I-labelled Re-chemotype LPS to mouse macrophage-like J774.1 cells to induce cytokine-release in J774.1 cells. LPS, synthetic Escherichia coli-type lipid A (compound 506) and tetraacyl percursor Ia (compound 406) inhibited the binding of 125I-LPS to macrophage-like J774.1 cells and induced the release of tumor ncerosis factor α (TNFα) and interleukin 6 (IL-6). Deacylated R-chemotype LPS preparations were completely inactive in inhibiting binding and in inducing cytokine-release. Among tetraacyl compounds, the inhibition-capacity of LPS-binding was in decreasing order: PE-4 (α-phosphonooxyethyl analogue of 406)〉406⪢〉404(4′-monophosphoryl partial structure of 406)〉405 (1-monophosphoryl partial structure of 406). In the case of hexaccyl preparations, compounds 506, PE-1 (α-phosphonooxyethyl analogue of 506) and PE-2 (differing from PE-1 in having 14:0 at positions 2 and 3 of the reducing GlcN) inhibited LPS-binding and induced cytokine release equally well, whereas preparation PE-3 (differing from PE-2 in containing a β-phosphhonooxyethyl group) showed a substantially lower capacity in binding-inhibition and cytokine-induction. The conclusion is that chemical changes in the hydrophilic lipid A backbone reduce the capacity of lipid A to bind to cells, whereas the number of fatty acids determines the capacity of lipid A to activate cells. These results indicate that the bisphosphorylated hexosamine backbone of lipid A is essential for specific binding of LPS to macrophages and that the acylation pattern plays a critical role for LPS-promoted cell activation, i.e. cytokine induction.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1574-695X.1994.tb00421.x
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 5
    Electronic Resource
    Electronic Resource
    Antibody response to MfGL-II, a phosphocholine-containing major lipid of Mycoplasma fermentans membranes (1997)
    Oxford, UK : Blackwell Publishing Ltd
    FEMS microbiology letters 154 (1997), S. 0 
    Details
    ISSN: 1574-6968
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology
    Notes: The choline-containing phosphoglycolipid, MfGL-II, is the major polar lipid of Mycoplasma fermentans PG18. Anti-MfGL-II antisera raised in rabbits using the purified MfGL-II as an immunogen were employed in immunogold electron microscopic and immunofluorescence studies showing that MfGL-II is uniformly distributed and exposed on the cell surface of M. fermentans cells. The specificity of the antibodies was determined by immunostaining of lipid extracts separated by thin layer chromatography. The antibodies recognize lipids specific to M. fermentans but did not cross-react with lipid extracts of M. penetrans, M. capricolum, M. gallisepticum or Acholeplasma laidlawii. As phosphocholine almost completely abolished antibody interaction with MfGL-II in an ELISA assay it is suggested that the anti-MfGL-II repertoire is composed primarily of anti-phosphocholine antibodies. The anti-MfGL-II antisera inhibit the attachment of M. fermentans to Molt-3 lymphocytes suggesting that MfGL-II plays a major role in M. fermentans-host cell interaction.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1574-6968.1997.tb12668.x
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 6
    Electronic Resource
    Electronic Resource
    The 5′-proximal hairpin loop of lbi RNA is a key structural element in repression of d-galactan II biosynthesis in Klebsiella pneumoniae serotype O1 (2000)
    Oxford, UK : Blackwell Science Ltd
    Molecular microbiology 36 (2000), S. 0 
    Details
    ISSN: 1365-2958
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Notes: The lbi (lipopolysaccharide biosynthesis interfering) RNA of phage Acm1, an untranslated RNA transcript of 97 nucleotides, previously shown to affect O-polysaccharide biosynthesis in various Escherichia coli strains, was found to downregulate the synthesis of the d-galactan II component of the O-specific polysaccharide in Klebsiella pneumoniae serotype O1. Enzymatic and Pb2+ probing experiments revealed that lbi RNA consists of two consecutive stem–loop structures, the 5′-proximal hairpin loop of 15 nucleotides being particularly accessible to single strand-specific probes. Based on the assumption that the 5′-proximal hairpin loop may be involved in an antisense interaction with cellular target RNAs, we randomly mutagenized one or two of its central nucleotides. Expression of mutated lbi RNA variants in K. pneumoniae serotype O1 relieved at least partly the repression of d-galactan II formation. In addition, a truncated version of lbi RNA lacking the 3′-proximal hairpin loop was almost as efficient as the wild-type RNA in downregulating d-galactan II synthesis. The results obtained indicate that the 5′-proximal hairpin loop of lbi RNA functions as a key structural element in the mechanism leading to the inhibition of d-galactan II biosynthesis in K. pneumoniae serotype O1.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2958.2000.01894.x
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 7
    Electronic Resource
    Electronic Resource
    A lethal role for lipid A in Salmonella infections (1998)
    Oxford BSL : Blackwell Science Ltd, UK
    Molecular microbiology 29 (1998), S. 0 
    Details
    ISSN: 1365-2958
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Notes: Salmonella infections in naturally susceptible mice grow rapidly, with death occurring only after bacterial numbers in vivo have reached a high threshold level, commonly called the lethal load. Despite much speculation, no direct evidence has been available to substantiate a role for any candidate bacterial components in causing death. One of the most likely candidates for the lethal toxin in salmonellosis is endotoxin, specifically the lipid A domain of the lipopolysaccharide (LPS) molecule. Consequently, we have constructed a Salmonella mutant with a deletion–insertion in its waaN gene, which encodes the enzyme that catalyses one of the two secondary acylation reactions that complete lipid A biosynthesis. The mutant biosynthesizes a lipid A molecule lacking a single fatty acyl chain and is consequently less able to induce cytokine and inducible nitric oxide synthase (iNOS) responses both in vivo and in vitro. The mutant bacteria appear healthy, are not sensitive to increased growth temperature and synthesize a full-length O-antigen-containing LPS molecule lacking only the expected secondary acyl chain. On intravenous inoculation into susceptible BALB/c mice, wild-type salmonellae grew at the expected rate of approximately 10-fold per day in livers and spleens and caused the death of the infected mice when lethal loads of approximately 108 were attained in these organs. Somewhat unexpectedly, waaN mutant bacteria grew at exactly the same rate as wild-type bacteria in BALB/c mice but, when counts reached 108 per organ, mice infected with mutant bacteria survived. Bacterial growth continued until unprecedentedly high counts of 109 per organ were attained, when approximately 10% of the mice died. Most of the animals carrying these high bacterial loads survived, and the bacteria were slowly cleared from the organs. These experiments provide the first direct evidence that death in a mouse typhoid infection is directly dependent on the toxicity of lipid A and suggest that this may be mediated via pro-inflammatory cytokine and/or iNOS responses.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2958.1998.00952.x
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 8
    Electronic Resource
    Electronic Resource
    Biochemistry and cell biology of bacterial endotoxins (1996)
    Oxford, UK : Blackwell Publishing Ltd
    FEMS immunology and medical microbiology 16 (1996), S. 0 
    Details
    ISSN: 1574-695X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1574-695X.1996.tb00126.x
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 9
    Electronic Resource
    Electronic Resource
    Modulation of lipopolysaccharide-induced production of tumor necrosis factor, interleukin 1, and interleukin 6 by synthetic precursor Ia of lipid A (1992)
    Oxford, UK : Blackwell Publishing Ltd
    FEMS microbiology letters 89 (1992), S. 0 
    Details
    ISSN: 1574-6968
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology
    Notes: Abstract Endotoxin (lipopolysaccharide, LPS) induces the production of mediators of inflammation, which exerts pathophysiological effects such as fever or shock in mammals. In the present study we have investigated the modulation of LPS by the synthetic non-active tetraacylated precursor Ia of lipid A (compound 406) in the induction of tumor necrosis factor (TNF), interleukin 1 (IL-1) and interleukin 6 (IL-6) in human peripheral blood mononuclear cells (PBMC) and in human peripheral blood monocytes (PBMo). PBMC stimulated with LPS released TNF in a concentration dependent manner. Release of biologically active TNF, IL-1 and IL-6 was first detectable 4 h after LPS stimulation. Compound 406 alone in all concentrations tested did not induce TNF, IL-1 or IL-6 release, intracellular TNF or IL-1β, or mRNA for TNF or IL-1. Added to PBMC 1 h before LPS compound 406 enhanced or suppressed TNF release and suppressed IL-1 and IL-6 release depending on the ratio of concentrations between stimulator (LPS) and modulator (compound 406). In contrast to LPS stimulation alone TNF, IL-1 and IL-6 release in presence of compound 406 was delayed and first detectable after 6 to 8 h. Compound 406 was able to suppress LPS-induced intracellular TNF and IL-1β in PBMC. Added to PBMo 1 h before LPS it totally inhibited the production of mRNA for TNF and IL-1. When added to PBMC 1 h after LPS, TNF release was suppressed in a concentration-dependent way and release of biologically active TNF, IL-1 and IL-6 could again be detected for the first time after 4 h. Compound 406 was not able to inhibit phorbol 12-myristate 13-acetate (PMA)-induced TNF and IL-1 release in PBMo which suggests that its modulating effect is LPS-specific. This study provides evidence that the modulating effect of compound 406 on the LPS induction of TNF, IL-, 1 and IL-6 could be due to competitive binding.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1574-6968.1992.tb04973.x
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 10
    Electronic Resource
    Electronic Resource
    Detection of lipopolysaccharide-binding proteins on membranes of murine lymphocyte and macrophage-like cell lines (1991)
    Oxford, UK : Blackwell Publishing Ltd
    FEMS microbiology letters 76 (1991), S. 0 
    Details
    ISSN: 1574-6968
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology
    Notes: Lipopolysaccharide-(LPS) binding proteins present on murine-lymphocyte and macrophage-like cell lines were identified by a ligand-blotting method and subsequent immunological detection of bound LPS. Membrane proteins of the murine-pre-B-cell line 70Z/3 were separated by SDS-PAGE, transferred electrophoretically onto nitrocellulose, and the blot was incubated with LPS of the Salmonella minnesota Re-mutant R595 (mRe-LPS). LPS bound to proteins on nitrocellulose was immunologically detected by anti-mRe-LPS antibodies; LPS was associated with one of the membrane proteins of 70Z/3 cells. This protein was 40 kDa under reducing and 45 kDa under non-reducing conditions, respectively. Treatment of 70Z/3 cells with pronase led to the disappearance of the LPS-binding protein indicating its surface location. Excess free lipid A, which represents the biologically active region of LPS, inhibited the binding of mRe-LPS to the protein. This LPS-binding protein was also identified on the pre-B-cell line CYG8, the B-cell line CYG101 and the murine-T-cell line BW5147. It was, however, not detectable on the B-cell line CYG34 and the myeloma-cell line P3-X63-Ag8.653. No other LPS-binding protein could be detected on these cell lines. In the murine-macrophage-like cell line J774.1, two LPS-binding proteins, one of 40 kDa and one of 80 kDa, were detected. These results indicate that mRe-LPS is specifically bound to a 40-kDa protein of lymphocytes, whereas in the case of macrophages it is associated with two LPS-binding proteins of 40 and 80 kDa.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1574-6968.1991.tb04257.x
    Location Call Number Limitation 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...