Browsing by Subject "Endotoxin"

Now showing 1 - 4 of 4
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    Alterations induced on cytoskeleton by Escherichia coli endotoxin in different types of rat liver cell cultures
    (Murcia : F. Hernández, 2003) Pagani, R.; Portolés, M.T.; De la Viña, S.; Melzner, I.; Vergani, G.
    Endotoxins (lipopolysaccharide, LPS) from Gram-negative bacteria are considered as the agents responsible for the induction of endotoxic shock, producing severe cellular metabolic dishomeostasis. Cytotoxic lesions, as well as functional and metabolic disturbances, occur mainly in the liver, which is one of the target organs and exerts an LPS clearance function. In an attempt to approach the molecular basis of endotoxic shock, and to propose an experimental model, we have focused this study on cytoskeleton (microtubules and microfilaments) alterations induced by different doses of endotoxin in different target liver cells. Microfilaments and microtubules were studied by immunofluorescence and different microscopy techniques (optic fluorescence microscopy and confocal laser scanning microscopy) in order to improve the cytoskeleton study resolution. Parenchymal and sinusoidal cell morphology, severely damaged by the LPS action, is related to a disturbance on the cytoskeletal organisation, even more evident in a particular proliferating rat liver cell culture. The most relevant changes are seen in the microtubule patterns in all liver cells tested, which could be related, depending on cell type, either to a direct LPS action or to [Ca+2]i dishomeostasis as well as free radical and cytokine (IL-1ß and TNF-a) production. Due to their features, proliferating rat liver cell cultures are used as a sensitive cell model to understand the effect of LPS on cytoskeleton organisation.
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    Artemisia pollen is the main vector for airborne endotoxin
    (Elsevier, 2018-08-09) Oteros, José; Bartusel, Elke; Alessandrini, Francesca; Núñez, Andrés; Moreno, Diego A.; Behrendt, Heidrun; Schmidt-Weber, Carsten; Traidl-Hoffmann, Claudia; Buters, Jeroen; Genética y Microbiología
    Background: Endotoxin (LPS) released from gram-negative bacteria causes strong immunologic and inflammatory effects and, when airborne, can contribute to respiratory conditions, such as allergic asthma. Objectives: We sought to identify the source of airborne endotoxin and the effect of this endotoxin on allergic sensitization. Methods: We determined LPS levels in outdoor air on a daily basis for 4 consecutive years in Munich (Germany) and Davos (Switzerland). Air was sampled as particulate matter (PM) greater than 10 μm (PM > 10) and PM between 2.5 and 10 μm. LPS levels were determined by using the recombinant Factor C assay. Results: More than 60% of the annual endotoxin exposure was detected in the PM > 10 fraction, showing that bacteria do not aerosolize as independent units or aggregates but adhered to large particles. In Munich 70% of annual exposure was detected between June 12th and August 28th. Multivariate modeling showed that endotoxin levels could be explained by phenological parameters (ie, plant growth). Indeed, days with high airborne endotoxin levels correlated well with the amount of Artemisia pollen in the air. Pollen collected from plants across Europe (100 locations) showed that the highest levels of endotoxin were detected on Artemisia vulgaris (mugwort) pollen, with little on other pollen. Microbiome analysis showed that LPS concentrations on mugwort pollen were related to the presence of Pseudomonas species and Pantoea species communities. In a mouse model of allergic disease, the presence of LPS on mugwort pollen was needed for allergic sensitization. Conclusions: The majority of airborne endotoxin stems from bacteria dispersed with pollen of only one plant: mugwort. This LPS was essential for inducing inflammation of the lung and allergic sensitization.
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    Electron microscopic study of the effects of endotoxin on the cells of the hepatic sinusoid in normal and BCG sensitized mice
    (Murcia : F. Hernández, 1991) McCuskey, Patricia A.; McCuskey, Robert S.
    Electron microscopic studies were conducted to access ultrastructural alterations in Kupffer cells and other cells lining the hepatic sinusoids at the peak of mediator release two hours after challenge with low doses of endotoxin under various conditions including reticuloendothelial system (RES) expansion and activation with BCG. BCG is known to sensitize animals to endotoxin rendering normally innocuous, low doses of endotoxin lethal. Low non-lethal doses (5 pg) of endotoxin activated Kupffer cells as well as caused isolated foci of cellular injury. However, animals which were treated with BCG had a highly activated and expanded RES system as evidenced by enlarged Kupffer cells with many extended cellular processes. Granulomas were prevalent and many reactive cells were present. After two hours marked cellular injury occurred to sinusoid lining and parenchymal cells when BCG treated animals were challenged with these same low doses of endotoxin. Cellular debris, fibrin, and platelets were observed in sinusoids often associated with Kupffer cells. These results suggest that the functional state of Kupffer cells is an important determinant in the host response to endotoxin. While there appears to be an effective clearance of endotoxin; the release of mediators by the highly activated Kupffer cells can be toxic causing hepatocellular injury.
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    In vitro effects of hormones and autacoids on the hydrogen peroxide production and the morphology of endotoxin-activated rat peritoneal macrophages
    (Murcia : F. Hernández, 2003) Kondomerkos, D.J.; Kalamidas, Stefanos; Kotoulas, Othon B.
    Peritoneal macrophages activated in vitro by endotoxin exhibit alterations of their capability to produce hydrogen peroxide after phorbol ester stimulation when certain hormones or autacoids are present in the culture medium. They also show morphological changes, mainly concerning cell size and nuclear appearance. Agents known to increase the intracellular levels of cyclic AMP, e.g. adrenalin and PGE2 reduce the hydrogen peroxide production. Insulin, which is known to decrease cyclic AMP levels, produces opposite results. Agents postulated to act via phospholipase C, e.g. serotonin, augment the production of hydrogen peroxide. We assume that this form of modulation may represent a regulatory mechanism of macrophage activation.