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Apolipoprotein H, a new mediator in the inflammatory changes ensuring in jeopardised human myocardium.

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OBJECTIVE To investigate the presence of membrane "flip flop" in ischaemic human myocardium, we assessed depositions of apolipoprotein H (apoH; beta 2-glycoprotein 1) in ischaemic myocardium. Serum protein apoH can bind to negatively charged phospholipids and can also inhibit blood coagulation in

[Biosynthesis of phospholipids in the myocardium during the chronic inflammatory bronchopulmonary process].

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Incorporation of U-14C-glucose into individual phospholipids from heart tissue was studied during chronic bronchopulmonary inflammation in vivo. Incorporation of the glucose into diphosphatidylglycerols, phosphatidyl serine, phosphatidyl ethanolamine was decreased and into the sphingomyelins,

Pharmacologic modulation of inflammatory mediator release by rat mast cells.

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Current knowledge of the mechanism of inflammatory mediator release from mast cells is reviewed with particular reference to the role of cyclic nucleotides and calcium and their interrelationship with one another as defined by studies in highly purified rat peritoneal mast cells. Data are presented

The interaction of leukocytes and their hydrolases with bacteria in vitro and in vivo: the modification of the bactericidal and bacteriolytic reactions by cationic and anionic macromolecular substances and by anti-inflammatory agents.

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Acid hydrolases from extracts of human blood leucocytes lyse Staph.aureus, Staph.albus and Strep.faecalis in vitro. The leucocyte enzymes can be substituted by a lytic mixture which contains crude trypsin, lysolecithin, phospholipase C and lysozyme, which lyse other bacterial species, e.g. E.coli

Inflammatory cytokines and lipopolysaccharide induce Fas-mediated apoptosis in renal tubular cells.

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OBJECTIVE Increased susceptibility of the kidney to acute renal failure (ARF) in the setting of sepsis even in the absence of systemic hypotension is well known. In the hypothesis that the proinflammatory cytokines and lipopolysaccharide (LPS) in gram-negative sepsis can directly cause renal tubular

Fucoidan delays apoptosis and induces pro-inflammatory cytokine production in human neutrophils.

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Although some immune modulatory effects of fucoidan have been elucidated, the effects of fucoidan on the apoptosis and activation of human neutrophils have not been investigated. In this study, we demonstrated that fucoidan purified from the brown seaweed Undaria pinnatifilda delays spontaneous

RGD-anchored magnetic liposomes for monocytes/neutrophils-mediated brain targeting.

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Negatively charged magnetic liposomes were prepared using soya lecithin (Soya PC), cholesterol and phosphatidyl serine (PS) for their preferential presentation to circulating blood phagocytes (monocytes and neutrophils). PS ratio was optimized in terms of drug and magnetite loading, in vitro

Chemo-resistant melanoma sensitized by tamoxifen to low dose curcumin treatment through induction of apoptosis and autophagy.

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Melanoma is the deadliest form of skin cancer, which is notoriously aggressive and chemo-resistant, and for which there is little effective treatment available if it goes undetected. Curcumin from the turmeric spice (Curcuma longa) has long been used in Southeast Asian medicine to alleviate ailments

Cytotoxicity and cell cycle arrest induced by andrographolide lead to programmed cell death of MDA-MB-231 breast cancer cell line.

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BACKGROUND Breast cancer is considered as an increasing major life-threatening concern among the malignancies encountered globally in females. Traditional therapy is far from satisfactory due to drug resistance and various side effects, thus a search for complementary/alternative medicines from

Mouse IL-3 induces histamine release from mouse peritoneal mast cells.

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In this study, we have attempted to determine whether mouse peritoneal mast cells released histamine in response to IL-3. Recombinant mouse (m)IL-3 induced histamine release from mouse peritoneal mast cells in a dose-dependent fashion. Histamine release did not occur in the absence of phosphatidyl

Signalling shutdown strategies in aging immune cells.

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It is important for the resolution of inflammation that the number and activity of immune cells are reduced. Clearance of immune cells may be achieved by apoptosis and phagocytosis of cell fragments by macrophages. However, signalling shutdown by immune cells committed to apoptosis occurs early in

IgA1 protease from Neisseria gonorrhoeae inhibits TNFalpha-mediated apoptosis of human monocytic cells.

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The modulation of programmed cell death is a common theme in the patho-physiology of inflammation and infectious disease. The synthesis and secretion of an IgA1 protease is strictly associated with virulence of the Neisseria species. Here, we report on the inhibition of tumor necrosis factor alpha

Redox imbalance of red blood cells impacts T lymphocyte homeostasis: implication in carotid atherosclerosis.

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Oxidative stress and immune/inflammatory responses are key pathogenetic factors of atherosclerotic disease. In this contest, mechanisms that regulate survival and death of immune cells may be relevant. Previous studies have demonstrated that red blood cells (RBCs) are physiologically able to inhibit

Interferon-alpha/beta inhibits IgE-dependent histamine release from rat mast cells.

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Although mast cells and interferons are both involved in numerous immune and inflammatory responses, little is known about how microenvironmental factors such as interferons (IFNs) influence mast cell function. To study this question, sensitized peritoneal mast cells (greater than 98% purity)

Autoantibodies to phospholipids and brain extract in patients with the Guillain-Barre syndrome: cross-reactive or pathogenic?

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Guillain-Barre syndrome (GBS) is a transient neurological disorder characterized by an inflammatory demyelination of peripheral nerves. Although the pathogenesis of GBS has not been elucidated, there is increasing evidence pointing to an autoimmune etiology. We have studied the reactivity of GBS

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