5,293 research outputs found
”Fluvastatin treatment inhibits leucocyte adhesion and extravasation in models of complement-mediated acute inflamation”F.Fischetti, R. Carretta, G. Borotto, P. Durigutto, R. Bulla, P.L. Meroni, F. Tedesco.
No full textAbstract
Complement activation plays a relevant role in the development of tissue damage under inflammatory conditions, and clinical and experimental observations emphasize its contribution to inflammatory vasculitides. Statins have recently been shown to reduce cardiovascular morbidity independently of plasma cholesterol lowering and in vitro studies support a direct anti-inflammatory action of these drugs. The aim of this study was to verify the in vivo effect of fluvastatin on complement-mediated acute peritoneal inflammation. The effect of oral treatment with fluvastatin was investigated in normo-cholesterolaemic rats that received intraperitoneal injection of either yeast-activated rat serum (Y-act RS) or lipopolysaccharide to induce peritoneal inflammation monitored by the number of PMN recruited in peritoneal fluid washes. In addition, vascular adherence and extravasation of leucocytes were evaluated by direct videomicroscopy examination on mesentery postcapillary venules topically exposed to Y-act RS. The number of PMN in the peritoneal washes of rats treated with fluvastatin was 38% lower than that of untreated animals (P < 0.05) 12 h after LPS injection, and was even lower (56%) in rats treated with Y-act RS already 8 h after injection (P < 0.02). Firm adhesion to endothelium and extravasation of leucocytes evaluated under direct videomicroscopy observation were significantly inhibited in fluvastatin treated rats (77% and 72%, respectively; P < 0.01), 120 min after treatment with Y-act RS. Our results demonstrate that fluvastatin inhibits in vivo complement-dependent acute peritoneal inflammation and suggest a role for statins in preventing the inflammatory flares usually associated with complement activation in chronic diseases, such as SLE or rheumatoid arthritis
Supporting social innovation in food networks
No full textThis case illustrates the contribution of service design to the creation of a network of
food-related services as a way to support the sustainable development of agricultural
peri-urban areas which are critical areas lying between towns and rural surroundings
In this project service design has complemented regional and urban planning
disciplines and methods providing a specific perspective on food system relations
and interactions; the work has been directed by a new concept of agricultural
multifunctionality based on de-mediated distribution systems, and on short food
chains between the productive countryside and the city
Recent advances in antiphospholipid antibodies and antiphospholipid syndromes in pediatric populations
No full textIn recent years, antiphospholipid antibodies (aPL) and their associated clinical features have been recognized increasingly in various pediatric autoimmune and non-autoimmune diseases. Pathogenic mechanisms involved in pediatric antiphospholipid syndrome (APS) appear to be the same as in adults. However, since pediatric patients do not have prothrombotic risk factors present in adults, there clearly are differences in the spectrum of clinical findings. The frequency of aPL-related thrombotic events is generally low in pediatric populations. On the other hand, various commonly acquired infections are likely to be responsible for higher percentage of non-pathogenic and transient aPL in childhood. Such points have to be considered in clinical judgment of elevated aPL in children. In this review we summarize the recent data on the prevalence and clinical significance of aPL in neonates, children and adolescents
Do we need an international consensus statement on classification criteria for the antiphospholipid syndrome in the paediatric population?
No full textAnti-inflammatory and immunomodulating properties of statins. An additional tool for the therapeutic approach of systemic autoimmune diseases?
No full textCardiovascular diseases secondary to accelerated atherosclerosis are now accepted as a cause of mortality and morbidity in patients suffering from systemic lupus erythematosus and rheumatoid arthritis. More recently, atherosclerosis is emerging as one of the most serious complications in the anti-phospholipid syndrome, although large epidemiological studies, such as those performed in lupus and rheumatoid arthritis patients, have not been performed up to now. Classical risk factors (dislipidemia, hypertension, diabetes, smoking, etc.) and steroid therapy cannot completely explain the high prevalence of cardiovascular complications in systemic autoimmune diseases. Since the modern view defines atherosclerosis as a chronic inflammatory disorder, it has been suggested that systemic inflammation and soluble immune mediators (circulating autoantibodies, immune-complexes, complement activation products) might play a role in accelerating vessel pathology. The main target appears to be the endothelium because of its ability to switch to a pro-adhesive, pro-inflammatory and pro-coagulant surface in response to these mediators. Recent advances in the knowledge of the pharmacology of statins have indicated that these drugs rather than to be simple cholesterol lowering molecules display a pleiotropic effects on several mechanisms involved in the atherosclerotic plaque formation. Their anti-inflammatory activity and particularly their ability to downregulate endothelial cell activation induced by different stimuli strongly suggest their possible use in conditions in which the systemic inflammation and the endothelial activation/damage are thought to represent key pathogenic mechanisms
Autoimmune or auto-inflammatory syndrome induced by adjuvants (ASIA) : old truths and a new syndrome?
No full textThere has been considerable interest in the role of environmental factors and the induction of autoimmunity and the ways by which they facilitate loss of tolerance. Clearly both genetic and environmental factors are incriminated, as evidenced by the lack of concordance in identical twins and the relatively recent identification of the shared epitope in rheumatoid arthritis. In this issue a new syndrome called 'Asia'-autoimmune/auto-inflammatory syndrome induced by adjuvants has been proposed. It is an intriguing issue and one that is likely to be provocative and lead to further biologic and molecular investigation
Accelerated Atherosclerosis in Autoimmune Diseases
No full textAtherosclerosis (AS) is a chronic inflammatory disease of arterial vessels, leading to chronic and acute ischemic damage or hemorrhages in virtually any organ. Atherosclerotic plaque formation is the result of inflammatory processes that mediate lymphocyte and macrophage infiltration, lipid intra- and inter-cellular deposition, and eventually smooth muscle cell migration/proliferation and fibrosis. Adaptive and innate immune responses against exogenous as well as self-antigens cooperate in triggering such processes. The atherogenic processes may be magnified and accelerated in patients with autoimmune rheumatic diseases (AIRDs) because of the underlying immune abnormalities, the consequent systemic inflammation and the effects of some concomitant chronic therapies. As a matter of fact, accelerated AS is responsible for increased mortality and morbidity in almost all AIRDs, nowadays. Diagnostic strategies to detect early atherosclerotic lesions and to apply preventive therapeutical approaches have been proposed in order to avoid complications related to accelerated AS in AIRDs. © The Editor(s) (if applicable) and The Author(s), under exclusive license to Springer Nature Switzerland AG 2008, 2024
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