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Platelets as immune cells in physiology and immunopathology

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889197408 Year: Pages: 111 DOI: 10.3389/978-2-88919-740-8 Language: English
Publisher: Frontiers Media SA
Subject: Allergy and Immunology --- Medicine (General)
Added to DOAB on : 2016-04-07 11:22:02
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Are platelets cells? (Not everyone agrees, since they are non-nucleate). And if platelets are cells - which all specialists consider at the time being - are they immune cells? The issue that platelets participate in immunity is no longer debated; however, the issue that they are key cells in immunity is challenged. It has even been proposed a couple of years ago that platelets can present antigen to T-lymphocytes by using their HLA class I molecules. No one has the same functional definition of platelets. The ‘Frontiers Research Topic’- coordinators’ own view is that platelets are primarily repairing cells, what they do in deploying tools of physiological inflammation. This function is better acknowledged as primary hemostasis, i.e. platelet adherence to injured or wounded vessels, followed by activation, aggregation, and constitution of the initial clot. Platelets would thus repair damaged vascular endothelium; so doing, as they patrol to detect damages, they sense danger along the vascular arborescence. As the latter is immense, platelets get close to tissues, which are not allowed to them under ‘physiological’ conditions but are readily accessible in pathology. Platelets are equipped with a variety of Pathogen Recognition Receptors such as TLRs; they have a complete signalosome, which is functional until the phosphorylation of NFkB; they have been proved to retro-transcribe RNA and synthesize de novo proteins; etc. Platelets participate to inflammation along the whole spectrum: from physiological (tissue repair, healing) to acute/severe inflammation (as can be seen in e.g. sepsis). In general, platelets engage complex interactions with most infectious pathogens. We propose there to cover those topics - from physiology to pathology, that put platelets within cells that not only take place in-, but also are key players of-, innate immunity. The relation of platelets with adaptive immunity is even more complex. Not everyone is convinced that platelets present antigens; however, platelets influence adaptive immunity since they have mutual interactions with Dendritic cells, Monocytes/Macrophages, and B-lymphocytes (the key players of antigen presentation); they also have mutual interactions with T-lymphocytes, though is issue is less clearly deciphered. We propose to also cover these topics - or to present the forum. There is another issue which is medically relevant - speaking of physiology/physiopathology-: this is fetal maternal incompatibility of platelet specific antigens (the HPA system) and the likely formation of maternal antibodies that often injure the newborn with risks of severe thrombocytopenia and intracranial hemorrhage. We propose an update on this issue as well. Last, platelets are very special because they can be directly therapeutic (by transfusion), even when being offered by a generous blood donor displaying given genetic and phenotypic parameters to a patient/recipient in need, who also display his/her own genetic and phenotypic parameters, which - for a large part - differ from the donor's ones. Besides immunization - via mechanisms probably close to the fetal maternal platelet incompatibility, but likely not similar -, transfusion has allowed the identification of the tremendous capacity of platelets to mediate inflammation: we propose to conclude the Topics with this item/forum.

Keywords

platelets --- Infection --- Inflammation --- immunity

Regulation of Inflammation; Its Resolution and Therapeutic Targeting

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889453597 Year: Pages: 105 DOI: 10.3389/978-2-88945-359-7 Language: English
Publisher: Frontiers Media SA
Subject: Medicine (General) --- Allergy and Immunology
Added to DOAB on : 2018-02-27 16:16:45
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Inflammation is a fundamental protective mechanism and at the same time the driving force of a variety of major diseases in humans. Indeed, acute self-resolving inflammation usually plays a positive role for the host, as exemplified by infectious diseases where its positive role is well established and testified by its perception as innate immunity. On the other hand, non-resolving inflammation and consequent chronicization is a key determinant of immunopathology and clinical manifestations of most major diseases in humans. As a consequence, it is increasing appreciated that the problem with inflammation is not how often it starts, but how often it fails to resolve. Appropriate resolution of inflammatory responses, which also drives activation of tissue damage repair mechanisms and return of local tissues to homeostasis, is a necessary process for ongoing health. Interestingly, cells sustaining these processes are also key to the proinflammatory responses, and the underlying “pro-resolving” molecular pathways are triggered as part of the pro-inflammatory response. This clearly indicates resolution of inflammation as an active process requiring functional repolarization of inflammatory cells that calls our attention on the underlying molecular mechanisms. The increasing number of anti-inflammatory drugs best-sellers in the pharma market is a clear indication of the relevance of having inflammation under check; nonetheless, there is still a great need for better acting pharmacological tools for the control of inflammation. Indeed, the remarkable success of biological drugs targeting proinflammatory cytokines has indicates that tools able to block proinflammatory mediators have promising applications, but at the same time has made clear that there are intrinsic limitations to this approach which frequently vanish undermine the activity of single targeting drugs, including the well-known redundancy of inflammatory mediators. Under self-limiting conditions inflammation spontaneously resolves in an active process. Some cellular and molecular mechanisms involved in inflammation resolution have been uncovered in the recent past, and include generation of specific cytokines, apoptosis of inflammatory leukocytes, lipid mediators, macrophage repolarization and others are likely to be revealed in the next future, since loss-of-function mutations of an increasing number of genes results in the development of spontaneous inflammation in experimental animals. We argue that “pushing for“ inflammation resolution by exploiting active naturally-occurring pro-resolving processes may have significant advantages over the attempt to simply “push back” inflammation by passive blockade of proinflammatory mediators. At present the research in the field of inflammation aims at identifying and validates new molecules involved in the resolution of inflammation as a basis for the development of innovative therapeutic strategies in chronic inflammatory and autoimmune diseases. This involves the discovery of new natural or synthetic “pro-resolving” molecules from plant and animals and the investigation of endogenous inflammation “pro-resolving” mechanisms, including atypical chemokine receptors, decoy receptors, and microRNA. An extensive effort is focused on the regulation by “pro-resolving” agents on two molecular systems of key relevance in inflammation: the chemokine system, which regulates recruitment, permanence and egress of leukocyte in tissues; and the Toll Like Receptor (TLR)/IL-1R system, which is central for the activation of infiltrating leukocytes.

Nutrients, Infectious and Inflammatory Diseases

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ISBN: 9783038427919 9783038427926 Year: Pages: CCCXLVIII, 18 Language: English
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Internal medicine
Added to DOAB on : 2018-04-27 16:16:52
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Foodborne disease like salmonellosis and toxoplasmosis are amongst the most significant causes of hospitalization in the U.S. and globally. Gastrointestinal infections alter gut microbiomes and increase permeability to toxins. Various invasions by microbial, fungal, viral and parasitic agents stimulate inflammation, a defensive mechanism of the body’s immune system. Other stimuli include environmental stimuli, oxidative stress, aging and the physiological process. A long-lasting, persistent and excessive inflammatory response is a significant risk factor for developing various chronic inflammatory and infectious diseases.Different nutritional and dietary life styles, whether poor or lacking essential nutritional elements, as well as excess intake, can result in inflammatory complications and loss of function. Nutritional deficiency is linked with several infectious and inflammatory diseases as a cause or consequence. For instance, protein deficiency was reported in orphanages to provoke microbial and fungal complications including Pneumocystis pneumonia. Similarly, protein deficiency is a tell-tale sign of several parasitic diseases. Studies indicate that nutrients, such as amino acids, oligosaccharides, and short-chain fatty acids exert inhibitory and anti-inflammatory functions. These investigations help to understand nutritional contributions to the prevention, treatment and taming of certain inflammatory and infectious diseases. Infectious and inflammatory complications go hand-in-hand with malnutrition.The purpose of this Special Issue is to publish related new, basic and translational findings and clinical trials in this area. Other investigations or review articles were sought to link infectious and inflammatory diseases with nutrients. In addition, novel diagnostic, preventive and therapeutic modalities were invited to aid the development of nutritional strategies for the treatment and/or prevention of inflammation and infection. Original reviews were of particular interest to advance our understanding of signaling pathways, and the molecular and biochemical mechanisms behind the effects of nutrients on inflammatory and infectious diseases.

New Translational Insights on Metabolic Syndrome: Obesity, Hypertension, Diabetes and Beyond

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889199242 Year: Pages: 114 DOI: 10.3389/978-2-88919-924-2 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Physiology
Added to DOAB on : 2016-01-19 14:05:46
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Metabolic syndrome (MetS) can be considered as a clustering of several risk factors such as obesity, hypertension, insulin resistance and dyslipidemia, which could lead to the development of diabetes and cardiovascular diseases (CVD). There are several underlying causes for MetS including overweight, physical inactivity and genetic factors. However, the underlying mechanisms that leads to MetS are still poorly understood. Therefore, the aim of this E-book is to provide a space where researchers holding different backgrounds could shed some light onto the pathophysiology of different risk factors involved in MetS, mostly from translational research worldwide.

Innate immunity and neurodegenerative disorders

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889193103 Year: Pages: 87 DOI: 10.3389/978-2-88919-310-3 Language: English
Publisher: Frontiers Media SA
Subject: Psychiatry --- Therapeutics --- Neurology --- Medicine (General) --- Science (General)
Added to DOAB on : 2016-02-05 17:24:33
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Inflammation of the brain in the context of neurodegenerative disorders is an area of intense debate and discussion, not least in terms of its pathogenic significance and the extent to which it drives disease processes and pathology. This inflammation can take several forms including innate responses recruiting microglia, humoral responses involving antibody, complement mediated processes and cellular T-cell activation, of which the role and extent of each may differ between diseases. Whilst some diseases have been more intensely linked to inflammation and long-term degeneration (e.g. MS), more traditional chronic neurodegenerative disorders have been thought of in terms of intrinsic neuronal pathology with a secondary innate response. However, it has been described that microglia activation is an early event of many degenerative disorders and evidence is accumulating that it may play a critical role in actually causing pathology and driving disease processes. If true, this would have major therapeutic implications, but what is the evidence that this is the case? The initial observations by Patrick McGeer’s group of post-mortem tissue from patients with Parkinson’s disease revealed the presence of activated brain microglia and has thus lead to the hypothesis that chronic inflammation could participate to neuronal degenerative processes. The significance of these original observations has only been recently revisited, and the development of more powerful tools to study the brain immune response has certainly contributed to this field of research. Chronic inflammation in the brain can take many forms but of particular interest has been the resident microglia and the role they play in this process. In this context, microglia have often been thought to become activated only after the disease has begun and then to contribute minimally to the degenerative process. Emerging new concepts challenge this view by proposing that microglial senescence, for example, may release the disease process and/or accelerate it. In addition, microglia, once activated, can adopt different phenotypes which can be both pro-inflammatory and pro-repair and may impact not only on the healthy adult neuronal population but on those new neurons derived from neurogenic niches of the adult brain. In this Research Topic, we attempt to explore this by first considering the innate immune responses in the brain and the methods by which they can be studied experimentally and in patients with various neurodegenerative disorders. This sets the scene for then discussing a range of different disorders including Alzheimer’s, Parkinson’s, Huntington’s disease and amyotrophic lateral sclerosis. These papers seek to discuss the evidence for an innate immune response and whether this is beneficial or detrimental, as well as its therapeutic implications.

HSPs - Ambiguous Mediators of Immunity

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889451524 Year: Pages: 92 DOI: 10.3389/978-2-88945-152-4 Language: English
Publisher: Frontiers Media SA
Subject: Allergy and Immunology --- Medicine (General)
Added to DOAB on : 2017-08-28 14:01:09
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Heat shock proteins (HSPs) were discovered as polypeptides induced by stress that can be found in all kingdoms of cellular organisms. Their functions were, a first enigmatic and these proteins were thus classified by molecular weight, as in—Hsp27, Hsp70, Hsp90, Hsp110. More recently, each of these size-classified molecules has attributed a role in protein folding, and they thus came to be known, as a class, as molecular chaperones. However, the they possess properties beyond chaperoning. Indeed, their discovery in the extracellular spaces suggested roles in regulation of the immune responses.

Cardiac Remodeling: New Insights in Physiological and Pathological Adaptations

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889453313 Year: Pages: 117 DOI: 10.3389/978-2-88945-331-3 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Physiology
Added to DOAB on : 2018-02-27 16:16:45
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The effective management of Cardiac remodeling(CR), remains a major challenge. Heart failure remains the leading cause of death in industrialized countries. Yet, despite the enormity of the problem, effective therapeutic interventions remain elusive. In fact, several initially promising agents were found to decrease mortality in patients recovering from myocardial infarction. Cardiac remodeling is defined as molecular and interstitial changes, manifested clinically by changes in size, mass , geometry and function of the heart in response to certain aggression. Initially, ventricular remodeling aims to maintain stable cardiac function in situations of aggression.

Macrophages Role in Integrating Tissue Signals and Biological Processes in Chronic Inflammation and Fibrosis

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889453320 Year: Pages: 104 DOI: 10.3389/978-2-88945-332-0 Language: English
Publisher: Frontiers Media SA
Subject: Medicine (General) --- Allergy and Immunology
Added to DOAB on : 2018-02-27 16:16:45
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Macrophages comprehend a heterogeneous mononuclear phagocytic population with wide range phenotypes and roles in homeostasis maintenance and diseases, such as infections, autoimmunity and cancer. Technology improvements enable researchers to track different macrophage populations in different tissues and situations and hypothesize on their role in promoting inflammation or stimulating tissue repair. Through innate immune recognition system macrophages can launch several effector artilleries that culminate in the production of various types of inflammatory mediators as cytokines, chemokines, lipid mediators and oxygen reactive species, which in turn, influence the behavior of other cells. Furthermore, macrophages and interacting cells are also susceptible to metabolic changes that ultimately will define the outcome macrophage signaling and its effect in the tissue. Here, we present a concise series of discussions on the role of macrophages, its response to the microenvironment and effects on other cells during tissue injury and repair. Triggering of inflammasome in macrophage activation and function is of special interest in this issue. We will emphasize the role of different macrophage subpopulations and the plasticity of these cells during fibrotic process in different models of diseases.

Inflammation in the CNS: Advancing the Field Using Intravital Imaging

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889453641 Year: Pages: 108 DOI: 10.3389/978-2-88945-364-1 Language: English
Publisher: Frontiers Media SA
Subject: Medicine (General) --- Allergy and Immunology
Added to DOAB on : 2018-02-27 16:16:45
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Inflammation of the CNS can have devastating, long-lived, and in some cases fatal consequences for patients. The stimuli that can induce CNS inflammation are diverse, and include infectious agents, autoimmune responses against CNS-expressed antigens, and sterile inflammation following ischemia or traumatic injury. In these conditions, cells of the immune system play central roles in promulgation and resolution of the inflammatory response. However, the immunological mechanisms at work in these diverse responses differ according to the nature of the response. Our understanding of the actions of immune cells in the CNS has been restricted by the difficulty in visualising leukocytes as they undergo recruitment from the cerebral microvasculature and following their entry into the CNS parenchyma. However, advances in in vivo microscopy over the last 10-15 years have overcome many of these difficulties, and studies using these forms of microscopy have revealed a wealth of new information regarding the cellular and molecular mechanisms of CNS inflammation. This Research Topic brings together state of the art reviews examining the use of in vivo imaging in investigating inflammation and leukocyte behaviour in the CNS. Papers in this Research Topic describe how in vivo microscopy has increased our understanding of the actions of immune cells in the inflamed CNS, following various stimuli including autoimmunity, infection and sterile inflammation.

Microglia in Health and Disease: A Unique Immune Cell Population

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889456017 Year: Pages: 108 DOI: 10.3389/978-2-88945-601-7 Language: English
Publisher: Frontiers Media SA
Subject: Medicine (General) --- Neurology --- Allergy and Immunology
Added to DOAB on : 2019-01-23 14:53:43
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Microglia are essential for the development and function of the adult brain. Their ontogeny, together with the absence of turnover from the periphery and the singular environment of the central nervous system (CNS), make microglia a unique cell population compared to other tissue-macrophages. The unique properties and functions of microglial cells, such as their role in synaptic pruning or the exceptional capacity to scan the brain parenchyma and rapidly react to its perturbations, have emerged in recent years. In the coming years, understanding how microglia acquire and maintain their unique profiles in order to fulfil distinct tasks in the healthy CNS and how these are altered in disease, will be essential to develop strategies to diagnose or treat CNS disorders with an immunological component.This Research Topic covers several aspects of microglial biology, ranging from their origin and the functional role of microglia during development and lifespan, their molecular properties compared with other brain and peripheral immune cells to microglial phenotypes and functional states in neurodegenerative diseases and brain tumours. In conclusion, the present Research Topic provides a comprehensive overview of our current understanding of several cellular and molecular mechanisms that make microglia a unique immune cell population within the healthy CNS as well as under inflammatory, neurodegenerative and tumorigenic processes.

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