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| 2. |
- Hall, Maria, et al.
(författare)
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The predatory mite Hypoaspis aculeifer is attracted to food of its fungivorous prey
- 1999
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Ingår i: Pedobiologia. - 0031-4056. ; 43:1, s. 11-17
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Tidskriftsartikel (refereegranskat)abstract
- To locate a prey a predator may rely on information originating from the habitat or the food of the prey, from the prey itself or its feeding activities. This study examines the origin of information used by the soil living predatory mite Hypoaspis aculeifer (Canestrini) when foraging for a fungivorous collembolan prey Folsomia f metaria (L.). Preference experiments were performed in Petri dishes, where the mite chose between fungal or agar cores with or without prey traces. The mite was attracted to fungi, but not to prey-related cues or other cues induced by grazing of collembolans. This suggests a foraging strategy of a generalist predator that mainly relies on fungal stimuli that lead to an area, where the probability of encountering fungivorous prey is high.
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| 3. |
- Hedlund, Maria, et al.
(författare)
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Role of the ceramide signalling pathway in cytokine responses to P fimbriated Escherichia coli.
- 1996
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Ingår i: Journal of Experimental Medicine. - : Rockefeller University Press. - 1540-9538 .- 0022-1007. ; 183:3, s. 1037-1044
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Tidskriftsartikel (refereegranskat)abstract
- Escherichia coli express fimbriae-associated adhesins through which they attach to mucosal cells and activate a cytokine response. The receptors for E. coli P fimbriae are the globoseries of glycosphingolipids; Gal alpha 1-->4Gal beta-containing oligosaccharides bound to ceramide in the outer leaflet of the lipid bilayer. The receptors for type 1 fimbriae are mannosylated glycoproteins rather than glycolipids. This study tested the hypothesis that P-fimbriated E. coli elicit a cytokine response through the release of ceramide in the receptor-bearing cell. We used the A498 human kidney cell line, which expressed functional receptors for P and type 1 fimbriae and secreted higher levels of interleukin (IL)-6 when exposed to the fimbriated strains than to isogenic nonfimbriated controls. P-fimbriated E. coli caused the release of ceramide and increased the phosphorylation of ceramide to ceramide 1-phosphate. The IL-6 response to P-fimbriated E. coli was reduced by inhibitors of serine/threonine kinases but not by other protein kinase inhibitors. In contrast, ceramide levels were not influenced by type 1-fimbriated E. coli, and the IL-6 response was insensitive to the serine/threonine kinase inhibitors. These results demonstrate that the ceramide-signaling pathway is activated by P-fimbriated E. coli, and that the receptor specificity of the P fimbriae influences this process. We propose that this activation pathway contributes to the cytokine induction by P-fimbriated E. coli in epithelial cells.
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| 4. |
- Hedlund, Maria, et al.
(författare)
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Sphingomyelin, glycosphingolipids, and ceramide signalling in cells exposed to p-fimbriated Escherichia coli
- 1998
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Ingår i: Molecular Microbiology. - : Wiley. - 1365-2958 .- 0950-382X. ; 29:5, s. 1297-1306
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Forskningsöversikt (refereegranskat)abstract
- Uropathogenic Escherichia coli attach to epithelial cells through P fimbriae that bind Galα1‐4Galβ‐oligosaccharide sequences in cell surface glycosphingolipids. The binding of P‐fimbriated E. coli to uroepithelial cells causes the release of ceramide, activation of the ceramide signalling pathway and a cytokine response in the epithelial cells. The present study examined the molecular source of ceramide in human kidney A498 cells exposed to P‐fimbriated E. coli. Agonists such as TNF‐α and IL‐1β released ceramide from sphingomyelin by the activation of endogenous sphingomyelinases and hydrolysis of sphingomyelin, and triggered an IL‐6 response. P‐fimbriated E. coli caused a slight increase in endogenous sphingomyelinase activity, but there was no associated sphingomyelin hydrolysis. Instead, the concentration of galactose‐containing glycolipids decreased. We propose that P‐fimbriated E. coli differ from other activators of the ceramide pathway, in that release of ceramide is from receptor glycolipids and not from sphingomyelin. Receptor breakdown may be an efficient host defence strategy, as it reduces the concentration of cell surface receptors, releases soluble receptor analogues and activates an inflammatory response.
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| 5. |
- Johansson, Erik, et al.
(författare)
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PHOTOVOLTAIC AND INTERFACIAL PROPERTIES OF HETEROJUNCTIONS COMPRISING DYE-SENSITIZED DENSE TiO2 AND TRIARYLAMINE DERIVATIVES IN SOLID AND LIQUID STATE.
- 1996
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Konferensbidrag (övrigt vetenskapligt/konstnärligt)abstract
- Different triarylamine derivatives have successfully been used as solid hole-conductor materials in dye-sensitized solar cells with efficiencies up to 4% [1-3]. In the present work TiO2/dye/ hole-conductor heterojunctions is assembled to form model systems for solid state DSSC and the interfacial structure at the molecular level. A series of triarylamine molecules is used to investigate the influence of small differences in the hole-conductor material structure on the photovoltaic and molecular surface properties. Both solid state and liquid state junctions with the triarylamine molecules were investigated. In the solid state heterojunctions the hole-conductor molecules were evaporated on the substrate and in the liquid state heterojunctions the hole-conductor molecules were solvated in an organic solvent. The photovoltaic properties of the heterojunction largely depend on the electron transfer rates at the interfaces between the different materials (semiconductor, dye and hole-conductor). Photoelectron Spectroscopy (PES) measurements was used to investigate the molecular and electronic interface structure. In the figure below the valence electronic structure of interfaces with the different hole-conductors are shown.From the valence PES the interaction and the energy level matching between the dyes and the hole-conductors is studied. The results show large differences in the energy matching of the different holconducting materials with respect to the dye molecules partly explaining the differences in efficiency. The valence structure also shows that when combining different materials their individual properties adjust slightly to their new environment. From the core level PES we observe differences molecular surface structure. Specifically it was found that the smaller holecondctors are able to penetrate the dye layer and contact the TiO2 surface.
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| 6. |
- Svanborg, Catharina, et al.
(författare)
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Bacterial adherence and mucosal cytokine responses : Receptors and transmembrane signaling
- 1996
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Ingår i: Ann NY Acad Sci. - : Wiley. ; 797, s. 177-190
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Forskningsöversikt (refereegranskat)abstract
- By attaching to cells or secreted mucosal components, microbes are thought to avoid elimination by the flow of secretions that constantly wash mucosal surfaces. The attached state enhances their ability to trap nutrients and allows the bacteria to multiply more efficiently than do unattached bacterial cells. Attachment is therefore regarded as an end result in itself, and emphasis has been placed on the role of adherence for colonization of mucosal surfaces. Specific adherence was shown to be essential for the tissue tropism that is to guide microbes to their respective sites of colonization/infection. Attachment is not only a mechanism of tissue targeting but also a first step in the pathogenesis of many infections. The attaching bacteria engage in a 'cross-talk' with the host cells through the mutual exchange of signals and responses. Enteropathogenic E. coli induce attaching and effacing lesions. Shigella and Listeria sp. invade the cells and cause actin polymerization. This review describes the ability of bacteria to trigger mucosal inflammation through activation of cells in the mucosal lining. The results suggest that receptors for bacterial adhesins bind their ligands with a high degree of specificity and that ligand-receptor interactions trigger transmembrane signaling events that cause cell activation. Receptors for microbial ligands thus appear to fulfill also the same criteria as those used to define receptors for other classes of ligands such as hormones, growth factors, and cytokines.
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| 7. |
- Svanborg, Catharina, et al.
(författare)
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Cytokine responses during mucosal infections: role in disease pathogenesis and host defence
- 1999
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Ingår i: Current Opinion in Microbiology. - 1879-0364. ; 2:1, s. 99-103
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Tidskriftsartikel (refereegranskat)abstract
- Mucosal pathogens use diverse and highly specific molecular mechanisms to activate mucosal inflammation. It may even be argued that their virulence depends on the inflammatory response that they induce. Some bacteria target epithelial cells and trigger them to produce inflammatory mediators but others cross the mucosa and activate macrophages or dendritic cells. Although systemic release of inflammatory mediators causes many symptoms and signs of infection, local chemokine production leads to the recruitment of inflammatory cells and lymphocytes that participate directly in the clearance of bacteria from mucosal sites. In this way, mucosal inflammation is a two-edged sword responsible for disease associated tissue destruction and crucial for the antimicrobial defence. Understanding of these pathways should create tools to enhance the defence and interfere with disease.
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