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Various Inflammatory Mediators (various + inflammatory_mediator)
Selected AbstractsMelatonin prevents lipopolysaccharide-induced hyporeactivity in ratJOURNAL OF PINEAL RESEARCH, Issue 3 2004Roberta D'Emmanuele Di Villa Bianca Abstract:, Melatonin (MT) is the principal secretory product of the pineal gland and its role as an immumo-modulator is well established. Recent evidence shows that MT exerts protective effects in septic shock, hemorrhagic shock and inflammation. Lipopolysaccharide (LPS), from Escherichia coli, administered to animals directly stimulates a number of cells and systems to produce various inflammatory mediators. LPS-induced septic shock is characterized by hypotension and vascular hyporeactivity to contracting agents. In particular, the reactive oxygen species such as superoxide and nitric oxide (NO) contribute to the pathophysiology of septic shock. In this study, we demonstrate that MT pretreatment prevents the hyporeactivity to phenylephrine in vivo and in aorta rings collected from rats treated with the endotoxin. The beneficial effect of MT seems related to its antioxidant properties and with inhibition of inducible nitric oxide synthase (iNOS) protein expression, reduction of NO production and nitrotyrosine formation, in aorta, preventing vascular, and endothelial injury. Additionally, we first demonstrate, that MT inhibited nuclear enzyme poly (ADP-ribose) synthetase activation in vascular tissue. The current study underlined the protective effect of MT on the vascular dysfunction associated with septic shock, data that could support the clinical use of MT in human endotoxemia. [source] Regulation of Blood,Brain Barrier PermeabilityMICROCIRCULATION, Issue 2 2001WILLIAM G. MAYHAN ABSTRACT The blood-brain barrier minimizes the entry of molecules into brain tissue. This restriction arises by the presence of tight junctions (zonulae occludens) between adjacent endothelial cells and a relative paucity of pinocytotic vesicles within endothelium of cerebral arterioles, capillaries, and venules. Many types of stimuli can alter the permeability characteristics of the blood-brain barrier. Acute increases in arterial blood pressure beyond the autoregulatory capacity of cerebral blood vessels, application of hyperosmolar solutions, application of various inflammatory mediators known to be elevated during brain injury, and/or activation of blood-borne elements such as leukocytes can produce changes in permeability of the blood-brain barrier. The second messenger systems that account for increases in permeability of the blood-brain barrier during pathophysiologic conditions, however, remain poorly defined. This review will summarize studies that have examined factors that influence disruption of the blood-brain barrier, and will discuss the contribution of various cellular second messenger pathways in disruption of the blood-brain barrier during pathophysiologic conditions. [source] Increased production of cysteinyl leukotrienes and prostaglandin D2 during human anaphylaxisCLINICAL & EXPERIMENTAL ALLERGY, Issue 1 2009E. Ono Abstract Background Anaphylaxis is a life-threatening syndrome resulting from the sudden release of mast cell- and basophil-derived mediators into the circulation. However, pathological evidence of the association between inflammatory mediators and human anaphylaxis is insufficient. Objective The aim of this study was to better understand the relationship between in vivo production of inflammatory mediators and the pathogenesis of anaphylaxis. We also sought to evaluate mast cell activation in anaphylaxis. Methods We measured the concentrations of various inflammatory mediators in urine samples, which were collected from 32 anaphylactic patients during the onset of anaphlaxis and during clinical remission, 21 patients with asthma on acute exacerbation and 15 healthy control subjects. Blood and urine specimens were collected from the patients after provocation test. Urinary leukotriene E4 (LTE4), 9,, 11,-prostaglandin F2 (9,, 11,-PGF2), eosinophil-derived neurotoxin (EDN) and leukotriene B4 glucuronide (LTBG) concentrations were determined by enzyme immunoassay, and the activity of plasma platelet-activating factor acetylhydrolase and serum tryptase concentration were measured using commercially available kits. Results Significantly higher concentrations of urinary LTE4 and 9,, 11,-PGF2, which immediately decreased during clinical remission, were observed in the anaphylactic patients than in asthmatic patients on acute exacerbation and healthy control subjects. Concentrations of EDN and LTBG were not significantly different among the anaphylactic patients, asthmatic patients on acute exacerbation and healthy subjects. There was a significant correlation between urinary LTE4 and 9,, 11,-PGF2 concentrations in the anaphylactic patients (r=0.672, P=0.005, n=32). In addition, LTE4 concentration in patients with anaphylactic shock is significantly elevated compared with that in patients without anaphylactic shock. Conclusions This is a report on the significant increase in urinary LTE4 and 9,, 11,-PGF2 concentrations during anaphylaxis. Urinary LTE4 and 9,, 11,-PGF2 concentrations may be a reliable marker of endogenous production of inflammatory mediators associated with anaphylaxis. [source] Tumour necrosis factor-alpha (TNF- ,) enhances lymphocyte migration into rheumatoid synovial tissue transplanted into severe combined immunodeficient (SCID) miceCLINICAL & EXPERIMENTAL IMMUNOLOGY, Issue 1 2000S. Wahid Adhesion mechanisms play a major role in the recruitment of peripheral blood lymphocytes (PBL) which characteristically infiltrate rheumatoid arthritis (RA) synovium and other chronically inflamed tissues. Through a sequential series of complex integrated adhesion and signalling events, ,multistep model of migration', specific subsets of PBL are recruited into inflamed tissues. In this process both leucocyte receptors and microvascular endothelial (MVE) counter-receptors play a critical role. The MVE in particular, during an inflammatory state, is the target of various inflammatory mediators that cause the up-regulation of several cell adhesion molecules (CAM). One of the most important factors known to be a powerful inducer of MVE CAM is TNF- ,. Conversely, blocking TNF- , causes a down-modulation of CAM expression. To test directly the capacity of TNF- , to induce cell migration into RA synovium we adapted a model in which synovial grafts were implanted into SCID mice subcutaneously. Using this model we demonstrate that: (i) transplants remain viable and become vascularized and fed by mouse subdermal vessels; (ii) the mouse vasculature connects to the transplant vasculature which maintains the ability to express human CAM; (iii) intragraft injections of TNF- , up-regulate the expression of human CAM, following the down-regulation which occurred 4 weeks post-transplantation; and (iv) the up-regulation of graft CAM is associated with increased human PBL migration into the transplants. This study provides direct evidence in vivo of the capacity of TNF- , to induce cell migration. In addition, it provides the experimental background for the optimal use of this model. [source] | ||||||||||