trehalose/necroză

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Induction of pulmonary granulomas, macrophage procoagulant activity, and tumor necrosis factor-alpha by trehalose glycolipids.

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Trehalose 6,6' dimycolate (TDM), a mycobacterial glycolipid, induces granulomas and hemorrhagic toxic reactions when administered in oil but not as a suspension in saline. It was previously demonstrated by us that TDM forms highly structured layers at oil-water interfaces and then postulated that

Activation of protein kinase C by mycobacterial cord factor, trehalose 6-monomycolate, resulting in tumor necrosis factor-alpha release in mouse lung tissues.

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Cord factors are mycoloyl glycolipids in cell walls of bacteria belonging to Actinomycetales, such as Mycobacterium, Nocardia and Rhodococcus. They induce granuloma formation in the lung and interstitial pneumonitis, associated with production of macrophage-derived cytokines. We studied how cord

Induction of interferons (IFNs) and tumor necrosis factor (TNF) in mice by a novel glycolipid trehalose 2,3,6'-trimycolate from Rhodococcus aurantiacus (Gordona aurantiaca).

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The immunomodifying activity of a novel mycoloyl glycolipid, trehalose 2,3,6'-trimycolate (GaGM), from a unique psychrophilic acid-fast bacterium, Rhodococcus aurantiacus, was examined. ICR mice were primed intravenously (i.v.) or intraperitoneally (i.p.) with liposomes containing GaGM (300

A role for tumour necrosis factor-alpha, complement C5 and interleukin-6 in the initiation and development of the mycobacterial cord factor trehalose 6,6'-dimycolate induced granulomatous response.

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Trehalose 6,6'-dimycolate (TDM) is a glycolipid component of the mycobacterial cell wall that causes immune responses in mice similar to Mycobacterium tuberculosis (MTB) infection, including granuloma formation with production of proinflammatory cytokines. The precise roles of tumour necrosis factor

Participation of tumor necrosis factor in the antitumor activity of mycobacterial trehalose dimycolate (cord factor).

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Trehalose dimycolate, a mycobacterial glycolipid also known as cord factor, retains some of the antitumor properties of the intact BCG. Murine macrophages incubated in vitro in the presence of trehalose dimycolate for 20 h at 37 degrees C released a factor which was cytotoxic for the L929 tumor cell

Tumor necrosis factor is required for the priming of peritoneal macrophages by trehalose dimycolate.

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Trehalose dimycolate (TDM), a glycolipid present in the cell wall of Mycobacterium spp., is a powerful immunostimulant. We have developed an original model of macrophage activation where TDM is injected in vivo to prime peritoneal macrophages. These primed macrophages do not express inducible NO

Apatite nanoparticles mediate intracellular delivery of trehalose and increase survival of cryopreserved cells.

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Cryopreservation of tissue cells is an important method to maintain cell viability and cellular function. However, cell viability and function are less than ideal by conventional cell cryopreservation methods, which may result in apoptosis and necrosis of cells in cryopreservation. Trehalose plays a

Trehalose does not affect the functions of human neutrophils in vitro.

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OBJECTIVE Trehalose, naturally occurring disaccharide, has been reported to prevent postoperative abdominal adhesions in animal models. We investigated whether trehalose affects the function of human polymorphonuclear neutrophils (PMNs) in vitro to assess the feasibility of its clinical application

Trehalose alleviates PC12 neuronal death mediated by lipopolysaccharide-stimulated BV-2 cells via inhibiting nuclear transcription factor NF-κB and AP-1 activation.

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Inflammation is implicated in the pathogenesis of Parkinson's disease (PD). Trehalose is a disaccharide which exhibits a variety of effects like anti-aggregation, autophagy enhancement in PD. It has also been known to suppress inflammation in many experimental models, involving endotoxin shock,

Parallel antitumor, granuloma-forming and tumor-necrosis-factor-priming activities of mycoloyl glycolipids from Nocardia rubra that differ in carbohydrate moiety: structure-activity relationships.

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Multiple intravenous injections (30 micrograms, ten times) in ICR mice of trehalose dimycolate and glucose monomycolate from Nocardia rubra, containing C36-48 mycolic acids, showed a prominent antitumor effect on a subcutaneously implanted sarcoma-180, an allogeneic sarcoma of mice with a

The disaccharide trehalose inhibits proinflammatory phenotype activation in macrophages and prevents mortality in experimental septic shock.

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Proinflammatory phenotype activation in macrophages (MPhis) after sepsis orchestrates an inflammatory response leading to multiple organ dysfunction. Trehalose preserves cell viability during exposure to a range of environmental stresses. We investigated whether trehalose may inhibit

Lyophilized formulations of recombinant tumor necrosis factor.

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Recombinant tumor necrosis factor-alpha (TNF), an investigational biological response modifier, is a protein and is susceptible to particulate generation during handling in dilute aqueous solutions. TNF is prone to formation of nonreducible dimers and oligomers during formulation, lyophilization,

Glycoconjugate expression on the cell wall of tps1/tps1 trehalose-deficient Candida albicans strain and implications for its interaction with macrophages.

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The yeast Candida albicans has developed a variety of strategies to resist macrophage killing. In yeasts, accumulation of trehalose is one of the principal defense mechanisms under stress conditions. The gene-encoding trehalose-6-phosphate synthase (TPS1), which is responsible for trehalose

Trehalose promotes the survival of random-pattern skin flaps by TFEB mediated autophagy enhancement.

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Random-pattern skin flaps are commonly used and valuable tools in reconstructive surgery, however, post-operative random skin flap necrosis remains a major and common complication. Previous studies have suggested that activating autophagy, a major pathway for degradation of intracellular waste, may

Cytostatic product(s) released by activated macrophages, unrelated to interleukin 1, tumor necrosis factor alpha, and interferon-alpha/beta.

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Murine peritoneal macrophages activated for cytotoxicity by trehalose dimycolate in vivo and lipopolysaccharide in vitro released cytostatic factor(s) against EMT6 target cells, in 8-hr conditioned medium (CM). The cytostatic factor(s) completely blocked DNA synthesis by EMT6 cells within 16 hr.

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