7 resultados para bacterial membrane

em Deakin Research Online - Australia


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Two laboratory-scale membrane bioreactor systems were investigated to treat high saline wastewater containing 1,000 mg/L COD and 32 g/L NaCl, namely: the yeast membrane bioreactor (YMBR) and the bacterial membrane bioreactor (BMBR). COD removal of both processes was above 90% at a hydraulic retention time (HRT) of 5 hours (volumetric loading of 5 kg COD/m³.d), sludge retention time (SRT) of 50 days (the MLSS of above 14 g/L and the F/M of 0.4 d-1). Under these operating conditions, the YMBR could run at a ten-fold lower transmembrane pressure with significantly reduced membrane fouling rate compared to BMBR. This may be because of low production of adhesive extracellular polymers (ECP) and the secondary filtration layer formed from large yeast cells. ECP production of bacterial sludge was increased considerably at high salt concentrations (32 g/L and 45 g/L) and long SRTs. For the bacterial sludge, the increased salinity led to increase in ECP, whereas the ECP content of the yeast sludge was relatively small.

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Gram-negative bacterial peptidoglycan is specifically recognized by the host intracellular sensor NOD1, resulting in the generation of innate immune responses. Although epithelial cells are normally refractory to external stimulation with peptidoglycan, these cells have been shown to respond in a NOD1-dependent manner to Gram-negative pathogens that can either invade or secrete factors into host cells. In the present work, we report that Gram-negative bacteria can deliver peptidoglycan to cytosolic NOD1 in host cells via a novel mechanism involving outer membrane vesicles (OMVs). We purified OMVs from the Gram-negative mucosal pathogens: Helicobacter pylori, Pseudomonas aeruginosa and Neisseria gonorrhoea and demonstrated that these peptidoglycan containing OMVs upregulated NF-κB and NOD1-dependent responses in vitro. These OMVs entered epithelial cells through lipid rafts thereby inducing NOD1-dependent responses in vitro. Moreover, OMVs delivered intragastrically to mice-induced innate and adaptive immune responses via a NOD1-dependent but TLR-independent mechanism. Collectively, our findings identify OMVs as a generalized mechanism whereby Gram-negative bacteria deliver peptidoglycan to cytosolic NOD1. We propose that OMVs released by bacteria in vivo may promote inflammation and pathology in infected hosts.

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Bacteria use a variety of secreted virulence factors to manipulate host cells, thereby causing significant morbidity and mortality. We report a mechanism for the long-distance delivery of multiple bacterial virulence factors, simultaneously and directly into the host cell cytoplasm, thus obviating the need for direct interaction of the pathogen with the host cell to cause cytotoxicity. We show that outer membrane–derived vesicles (OMV) secreted by the opportunistic human pathogen Pseudomonas aeruginosa deliver multiple virulence factors, including b-lactamase, alkaline phosphatase, hemolytic phospholipase C, and Cif, directly into the host cytoplasm via fusion of OMV with lipid rafts in the host plasma membrane. These virulence factors enter the cytoplasm of the host cell via N-WASP–mediated actin trafficking, where they rapidly distribute to specific subcellular locations to affect host cell biology. We propose that secreted virulence factors are not released individually as naked proteins into the surrounding milieu where they may randomly contact the surface of the host cell, but instead bacterial derived OMV deliver multiple virulence factors simultaneously and directly into the host cell cytoplasm in a coordinated manner.

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Abstracts: Lipid rafts are defined as specialized, dynamic microdomains that can be found in plasma membrane, and they are enriched with cholesterol and sphingolipids. Since lipid rafts’ first debut in the mid 1990’s, their existence, function and biological relevance have been a subject of intense scrutiny within the scientific community. Throughout this debate, we have learned a great deal regarding how cargos (both pathogens and cellular factors) are transported into and out of the cell through raft-dependent or raft-independent pathways. It is now apparent that a number of toxins, bacterial-, and viral-pathogens are able to exploit cholesterol and/or lipid rafts to gain a foot hold in their target hosts. The objective of this review is to describe our current appreciation on how selected pathogens utilise cholesterol and/or lipid rafts to support their propagation and to speculate on how some of these observations can be explored for the development of novel strategies that target plasma membrane lipids to control the spread of these viral- and bacterial-pathogens.

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Mitochondrial fission requires the division of both the inner and outer mitochondrial membranes. Dynamin-related proteins operate in division of the outer membrane of probably all mitochondria, and also that of chloroplasts – organelles that have a bacterial origin like mitochondria. How the inner mitochondrial membrane divides is less well established. Homologues of the major bacterial division protein, FtsZ, are known to reside inside mitochondria of the chromophyte alga Mallomonas, a red alga, and the slime mould Dictyostelium discoideum, where these proteins are likely to act in division of the organelle. Mitochondrial FtsZ is, however, absent from the genomes of higher eukaryotes (animals, fungi, and plants), even though FtsZs are known to be essential for the division of probably all chloroplasts. To begin to understand why higher eukaryotes have lost mitochondrial FtsZ, we have sampled various diverse protists to determine which groups have retained the gene. Database searches and degenerate PCR uncovered genes for likely mitochondrial FtsZs from the glaucocystophyte Cyanophora paradoxa, the oomycete Phytophthora infestans, two haptophyte algae, and two diatoms – one being Thalassiosira pseudonana, the draft genome of which is now available. From Thalassiosira we also identified two chloroplast FtsZs, one of which appears to be undergoing a C-terminal shortening that may be common to many organellar FtsZs. Our data indicate that many protists still employ the FtsZ-based ancestral mitochondrial division mechanism, and that mitochondrial FtsZ has been lost numerous times in the evolution of eukaryotes.

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The invention provides a compound including : A core having a first face and a second face; A binding portion attached to the first face of the core, wherein the binding portion is capable of binding to an anionic group present in a cell membrane of a microorganism; and A hydrophobic portion attached to the second face of the core, wherein the hydrophobic portion is capable of interacting with the cell membrane of the microorganism; and The core comprises a dioxolane norbornane / norbornene of formula (II): Or a salt or ion thereof, wherein R' is a moiety forming part of a hydrophobic portion; R2 is a first binding portion; and R3 is a seconding binding portion. The invention also provides compositions including at least one such compound. The invention also provides methods and uses for treatment or prophylaxis of infection of a mammal by a microorganism, and methods and uses for treating or preventing contamination of a substrate by a microorganism, using the compounds and compositions.