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Anti-inflammatory Mediators  [PDF]
Madhukar Neerudu,Rajababu,Harinath Reddy,Pradeep Koppolu
Indian Journal of Dental Advancements , 2010,
Abstract: Lipoxins are a series of oxygenated arachidonic acid derivatives formed during cell to cell interactions and appear to function as endogenous anti-inflammatory mediators, they are trihydroxytetraene-containing lipid mediators and are predominantly counterregulators of some well-known mediators of inflammation. Since this circuit of lipoxin formation and action appears to be of physiological relevance for the resolution of inflammation, therapeutic modalities targeted at this system are likely to have fewer unwanted side effects than other candidates and current anti-inflammatory therapies. There is a growing appreciation that inflammation and its active resolution may be modulated by endogenously produced lipids. Recently, it was demonstrated that lipoxins are produced by peripheral blood neutrophils from patients diagnosed with aggressive periodontitis. The present paper focuses on the importance of lipoxins as anti-inflammatory mediators and their role in periodontal disease.
Requirements for Membrane Attack Complex Formation and Anaphylatoxins Binding to Collagen-Activated Platelets  [PDF]
Catherine Martel,Sylvie Cointe,Pascal Maurice,Sa?d Matar,Marta Ghitescu,Pierre Théroux,Arnaud Bonnefoy
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0018812
Abstract: The activation of complement during platelet activation is incompletely understood. Objectives: We sought to explore the formation of C5b-9 and anaphylatoxins binding to collagen-activated platelets.
The P2Y6 Receptor Mediates Clostridium difficile Toxin-Induced CXCL8/IL-8 Production and Intestinal Epithelial Barrier Dysfunction  [PDF]
Ashleigh Hansen, Laurie Alston, Sarah E. Tulk, L. Patrick Schenck, Michael E. Grassie, Basmah F. Alhassan, Arun Teja Veermalla, Samir Al-Bashir, Fernand-Pierre Gendron, Christophe Altier, Justin A. MacDonald, Paul L. Beck, Simon A. Hirota
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0081491
Abstract: C. difficile is a Gram-positive spore-forming anaerobic bacterium that is the leading cause of nosocomial diarrhea in the developed world. The pathogenesis of C. difficile infections (CDI) is driven by toxin A (TcdA) and toxin B (TcdB), secreted factors that trigger the release of inflammatory mediators and contribute to disruption of the intestinal epithelial barrier. Neutrophils play a key role in the inflammatory response and the induction of pseudomembranous colitis in CDI. TcdA and TcdB alter cytoskeletal signaling and trigger the release of CXCL8/IL-8, a potent neutrophil chemoattractant, from intestinal epithelial cells; however, little is known about the surface receptor(s) that mediate these events. In the current study, we sought to assess whether toxin-induced CXCL8/IL-8 release and barrier dysfunction are driven by the activation of the P2Y6 receptor following the release of UDP, a danger signal, from intoxicated Caco-2 cells. Caco-2 cells express a functional P2Y6 receptor and release measurable amounts of UDP upon exposure to TcdA/B. Toxin-induced CXCL8/IL-8 production and release were attenuated in the presence of a selective P2Y6 inhibitor (MRS2578). This was associated with inhibition of TcdA/B-induced activation of NFκB. Blockade of the P2Y6 receptor also attenuated toxin-induced barrier dysfunction in polarized Caco-2 cells. Lastly, pretreating mice with the P2Y6 receptor antagonists (MSR2578) attenuated TcdA/B-induced inflammation and intestinal permeability in an intrarectal toxin exposure model. Taken together these data outline a novel role for the P2Y6 receptor in the induction of CXCL8/IL-8 production and barrier dysfunction in response to C. difficile toxin exposure and may provide a new therapeutic target for the treatment of CDI.
Mediators of Inflammation in Acute Kidney Injury  [PDF]
Ali Akcay,Quocan Nguyen,Charles L. Edelstein
Mediators of Inflammation , 2009, DOI: 10.1155/2009/137072
Abstract: Acute kidney injury (AKI) remains to be an independent risk factor for mortality and morbidity. Inflammation is now believed to play a major role in the pathopathophysiology of AKI. It is hypothesized that in ischemia, sepsis and nephrotoxic models that the initial insult results in morphological and/or functional changes in vascular endothelial cells and/or in tubular epithelium. Then, leukocytes including neutrophils, macrophages, natural killer cells, and lymphocytes infiltrate into the injured kidneys. The injury induces the generation of inflammatory mediators like cytokines and chemokines by tubular and endothelial cells which contribute to the recruiting of leukocytes into the kidneys. Thus, inflammation has an important role in the initiation and extension phases of AKI. This review will focus on the mediators of inflammation contributing to the pathogenesis of AKI.
Inflammation Mediators: A Review  [cached]
L. S. Chauhan,C. S. Chauhan,C. P. Jain
Pharmaceutical Reviews , 2006,
Abstract: The inflammatory process involves a series of events that can be elicitedby numerous stimuli and provokes a characteristic pattern of responses. Ata microscopic level, the familiar clinical signs of erythema, edema, tenderness,and pain usually accompany the response.A substance that causes one of the component events in inflammation througha specific receptor is called a mediator of inflammation. Both endogenousand exogenous substances may acts as mediators e.g. proteins, lipids, histamine,serotonin, nitric oxide, endotoxin, interleukins, tumor necrosis factors etc.
Micrurus snake venoms activate human complement system and generate anaphylatoxins
Gabriela D Tanaka, Giselle Pidde-Queiroz, Maria de Fátima D Furtado, Carmen van den Berg, Denise V Tambourgi
BMC Immunology , 2012, DOI: 10.1186/1471-2172-13-4
Abstract: In the present study we have investigated the action of venoms from seven species of snakes from the genus Micrurus on the complement system in in vitro studies. Several of the Micrurus species could consume the classical and/or the lectin pathways, but not the alternative pathway, and C3a, C4a and C5a were generated in sera treated with the venoms as result of this complement activation. Micrurus venoms were also able to directly cleave the α chain of the component C3, but not of the C4, which was inhibited by 1,10 Phenanthroline, suggesting the presence of a C3α chain specific metalloprotease in Micrurus spp venoms. Furthermore, complement activation was in part associated with the cleavage of C1-Inhibitor by protease(s) present in the venoms, which disrupts complement activation control.Micrurus venoms can activate the complement system, generating a significant amount of anaphylatoxins, which may assist due to their vasodilatory effects, to enhance the spreading of other venom components during the envenomation process.The Elapidae family is represented in America by three genera of coral snakes: Micruroides, Leptomicrurus and Micrurus, the latter being the most abundant and diverse group. In Brazil, M. corallinus and M. frontalis are responsible for the majority of coral snake envenomations. Although, Micrurus bites are relatively rare, the accidents can cause death, by muscle paralysis and respiratory arrest, few hours after envenomation [1].The main feature of the coral snake action is the neurotoxicity, although, experimentally, it has been documented that some Micrurus venoms may produce myotoxicity and local lesions [2,3]. Furthermore, many enzymatic activities were detected in Micrurus venoms including phospholipase A2, hyaluronidase, phosphodiesterase, leucine amino peptidase, L-amino acid dehydrogenase and L-amino acid oxidase activities [4-6]. Only little or no proteolytic effects have been detected in Micrurus venoms [5,6].Previously, we have analyzed
Eosinophil recruitment and activation: the role of lipid mediators  [PDF]
Patrícia T. Bozza
Frontiers in Pharmacology , 2013, DOI: 10.3389/fphar.2013.00027
Abstract: Eosinophils are effector cells that migrate toward several mediators released at inflammatory sites to perform their multiple functions. The mechanisms driving eosinophil selective accumulation in sites of allergic inflammation are well-established and involve several steps controlled by adhesion molecules, priming agents, chemotactic, and surviving factors. Even though the majority of studies focused on role of protein mediators like IL-5 and eotaxins, lipid mediators also participate in eosinophil recruitment and activation. Among the lipid mediators with distinguish eosinophil recruitment and activation capabilities are platelet activating factor and the eicosanoids, including leukotriene B4, cysteinyl leukotrienes, and prostaglandin D2. In this review, we focused on the role of these four lipid mediators in eosinophil recruitment and activation, since they are recognized as key mediators of eosinophilic inflammatory responses.
Regulation of neutrophil trafficking by the lipid mediators of inflammation
S Marleau, J Lefebvre, H El Iman, C Bélanger, P Borgeat
Arthritis Research & Therapy , 2004, DOI: 10.1186/ar1346
Abstract: The objective of these studies is therefore to compare the role of each individual mediator and the collective effect of the three mediators in regulating neutrophil trafficking. Another objective is to assess whether or not the combined use of antagonists to the three classes of mediators could result in a stronger inhibitory effect on neutrophil trafficking.The studies are performed using potent and selective LTB4, LTD4 and PAF antagonists in both in vitro and in vivo models. The separate and collective role of the three classes of lipid mediators will be investigated in the migration of human neutrophils through a monolayer of human endothelial cells grown on a gel of extracellular matrix proteins. The studies also involve the use of models of dermal inflammation in rats and rabbits and the mouse air pouch model.The results show that, in the various models tested, neutrophil migration elicited by proinflammatory agents such as IL-1, tumor necrosis factor alpha and lipopolysaccharide is generally decreased by LTB4 or PAF antagonists, and that the combination of both antagonists results in a greater inhibitory effect, supporting the concept that several lipid mediators generated locally (at the blood–endothelium interface and/or at inflammatory sites) regulate neutrophil trafficking. Additional experiments involving antagonists to the three classes of lipid mediators, as well as LTB4 and PAF receptor knockout mice, are in progress.
Fibroblasts in fibrosis: novel roles and mediators  [PDF]
Ryan T. Kendall
Frontiers in Pharmacology , 2014, DOI: 10.3389/fphar.2014.00123
Abstract: Fibroblasts are the most common cell type of the connective tissues found throughout the body and the principal source of the extensive extracellular matrix (ECM) characteristic of these tissues. They are also the central mediators of the pathological fibrotic accumulation of ECM and the cellular proliferation and differentiation that occurs in response to prolonged tissue injury and chronic inflammation. The transformation of the fibroblast cell lineage involves classical developmental signaling programs and includes a surprisingly diverse range of precursor cell types—most notably, myofibroblasts that are the apex of the fibrotic phenotype. Myofibroblasts display exaggerated ECM production; constitutively secrete and are hypersensitive to chemical signals such as cytokines, chemokines, and growth factors; and are endowed with a contractile apparatus allowing them to manipulate the ECM fibers physically to close open wounds. In addition to ECM production, fibroblasts have multiple concomitant biological roles, such as in wound healing, inflammation, and angiogenesis, which are each interwoven with the process of fibrosis. We now recognize many common fibroblast-related features across various physiological and pathological protracted processes. Indeed, a new appreciation has emerged for the role of non-cancerous fibroblast interactions with tumors in cancer progression. Although the predominant current clinical treatments of fibrosis involve non-specific immunosuppressive and anti-proliferative drugs, a variety of potential therapies under investigation specifically target fibroblast biology.
Interleukin-1β and anaphylatoxins exert a synergistic effect on NGF expression by astrocytes
Anne-christine Jauneau, Alexander Ischenko, Alexandra Chatagner, Magalie Benard, Philippe Chan, Marie-therese Schouft, Christine Patte, Hubert Vaudry, Marc Fontaine
Journal of Neuroinflammation , 2006, DOI: 10.1186/1742-2094-3-8
Abstract: Injury in the CNS produces a multi-faceted, complex cascade of events that includes immunological changes such as activation of the complement system and generation of antibodies, release of pro-inflammatory cytokines and chemokines, and production of reactive oxygen species leading to oxidative stress. Activation of the complement (C) system leads to release of various fragments among which the anaphylatoxins, C3a and C5a, are two proinflammatory polypeptides. C3a and C5a, which are liberated through cleavage of C3 and C5 by C convertases, exert their biological activities by binding to two G protein-coupled receptors named C3aR and C5aR, respectively [1]. There is evidence that C biosynthesis occurs in the CNS and all components of the C system can be synthesized locally by astrocytes, microglia and neurons [2]. Complement functions to eliminate intruding pathogens. However, there is now considerable evidence that increased complement synthesis and uncontrolled complement activation in the CNS contribute to pathological changes in the brain. Intrathecal complement activation has been shown to occur in multiple sclerosis, Alzheimer's disease, bacterial meningitis, stroke and other brain diseases [3,4]. Inflammatory reactions in these disorders are also associated with expression of pro-inflammatory cytokines, including IL-1β, TNF-α, IL-6, IFN-γ and IL-8. Excess expression of these cytokines can result in the destruction of the body's own cells, particularly neurons.Several classes of neurons rely on neurotrophic factors, including nerve growth factor (NGF), for their survival and maintenance of function. Neurotrophins have many important physiological roles during and after CNS development [5]. Moreover, in brain disorders such as Alzheimer's disease increasing levels of endogenous NGF may be beneficial [6,7]. NGF is produced predominantly by neurons under normal physiological conditions; whereas astrocytes become the major site of NGF synthesis in the CNS during p
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