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phospholipase d/entzündung
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Seite 1 von 236 Ergebnisse
Resveratrol attenuates C5a-induced inflammatory responses in vitro and in vivo by inhibiting phospholipase D and sphingosine kinase activities.
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The anti-inflammatory activity of the phytoalexin resveratrol (RSV) was evaluated in C5 anaphylatoxin (C5a)-stimulated primary neutrophils and in a mouse model of acute peritonitis. Pretreatment of human and mouse neutrophils with RSV significantly blocked oxidative burst, leukocyte migration,
Rebamipide-induced downregulation of phospholipase D inhibits inflammation and proliferation in gastric cancer cells.
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Rebamipide a gastroprotective drug, is clinically used for the treatment of gastric ulcers and gastritis, but its actions on gastric cancer are not clearly understood. Phospholipase D (PLD) is overexpressed in various types of cancer tissues and has been implicated as a critical factor in
Effects of methylprednisolone and aprotinin on phospholipase D activity of leukocytes in systemic inflammatory response induced by cardiopulmonary bypass.
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OBJECTIVE
To investigate the role of leukocyte phospholipase D (PLD) in systemic inflammatory response induced by cardiopulmonary bypass (CPB) and the effects of methylprednisolone and aprotinin on leukocyte PLD activity.
METHODS
Forty-two patients who received CPB open heart surgery were divided
Changes in phospholipase D activity of leukocytes during human systemic inflammatory response syndrome induced by cardiopulmonary bypass.
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OBJECTIVE
To investigate the fluctuations in arterial leukocyte phospholipase D (PLD) activity during the perioperative period of open heart surgery under cardiopulmonary bypass (CPB), and the relationship between PLD activity and systemic inflammatory response induced by CPB.
METHODS
Arterial blood
[Phospholipase D and inflammation].
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Phospholipase D (PLD) is widely distributed in mammalian cells, where it is regulated by a variety of extracellular signals. Its major substrate is phosphatidylcholine (PC), which is hydrolyzed to phosphatidic acid (PA) and choline. The PLD-catalysed PC hydrolysis is believed to be an important
Phospholipase-D activity and inflammatory response induced by brown spider dermonecrotic toxin: endothelial cell membrane phospholipids as targets for toxicity.
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Brown spider dermonecrotic toxins (phospholipases-D) are the most well-characterized biochemical constituents of Loxosceles spp. venom. Recombinant forms are capable of reproducing most cutaneous and systemic manifestations such as dermonecrotic lesions, hematological disorders, and renal failure.
Expression of Phospholipase D in Periodontitis and Its Role in the Inflammatory and Osteoclastic Response by Nicotine- and Lipopolysaccharide-Stimulated Human Periodontal Ligament Cells.
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BACKGROUND
The aim of the present study is to investigate the expression of phospholipase D (PLD) 1 and PLD2 in periodontal patients and in human periodontal ligament cells (HPDLCs) exposed to nicotine plus lipopolysaccharide (LPS) from Porphyromonas gingivalis (Toll-like receptor 2 ligand).
New concepts in phospholipase D signaling in inflammation and cancer.
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Phospholipase D (PLD) catalyzes the hydrolysis of phosphatidylcholine to generate the lipid second messenger phosphatidic acid (PA) and choline. PLD regulation in cells falls into two major signaling categories. One is via growth factors/mitogens, such as EGF, PDGF, insulin, and serum, and
The phospholipase D pathway mediates the inflammatory response of the retinal pigment epithelium.
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The retinal pigment epithelium (RPE) plays an important immunological role in the retina and it is involved in many ocular inflammatory diseases that may end in loss of vision and blindness. In this work the role of phospholipase D (PLD) classical isoforms, PLD1 and PLD2, in the inflammatory
Novel polyisoprenyl phosphates block phospholipase D and human neutrophil activation in vitro and murine peritoneal inflammation in vivo.
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Leukocyte production of reactive oxygen species (ROS) is an essential component of the antimicrobial armament mounted during host defense, but when released to the extracellular milieu ROS can also injure host tissues and provoke inflammation. Polyisoprenyl phosphates (PIPPs) are constituents of
Functional regulation of phospholipase D expression in cancer and inflammation.
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Phospholipase D (PLD) regulates downstream effectors by generating phosphatidic acid. Growing links of dysregulation of PLD to human disease have spurred interest in therapeutics that target its function. Aberrant PLD expression has been identified in multiple facets of complex pathological states,
Chlamydophila pneumoniae phospholipase D (CpPLD) drives Th17 inflammation in human atherosclerosis.
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Phospholipases are produced from bacterial pathogens causing very different diseases. One of the most intriguing aspects of phospholipases is their potential to interfere with cellular signaling cascades and to modulate the host-immune response. Here, we investigated the role of the innate and
Forty Years of the Description of Brown Spider Venom Phospholipases-D.
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Spiders of the genus Loxosceles, popularly known as Brown spiders, are considered a serious public health issue, especially in regions of hot or temperate climates, such as parts of North and South America. Although the venoms of these arachnids are complex in molecular composition, often
IL-1 beta primes IL-8-activated human neutrophils for elastase release, phospholipase D activity, and calcium flux.
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Interleukin-8 (IL-8), the prototype of the alpha (e.i., C-X-C branch) chemokine family, induced elastase release in a concentration-dependent manner (50-1000 ng/mL) in cytochalasin B-treated human polymorphonuclear leukocytes (PMNs). This response was potentiated about twofold if PMNs were
Fc gamma receptor-mediated activation of phospholipase D regulates macrophage phagocytosis of IgG-opsonized particles.
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Receptors for the Fc portion of IgG (Fc gamma Rs) integrate the innate and acquired components of immunity by coupling the specific recognition of IgG Abs to the activation of phagocytic leukocytes. Knowledge of the molecular mechanisms that regulate phagocyte stimulation by Fc gamma Rs may permit
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