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The role of the immune system in the pathogenesis of diabetic complications

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889193523 Year: Pages: 95 DOI: 10.3389/978-2-88919-352-3 Language: English
Publisher: Frontiers Media SA
Subject: Nutrition and Food Sciences --- Neurology --- Science (General) --- Public Health --- Internal medicine --- Medicine (General)
Added to DOAB on : 2016-03-10 08:14:32
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The main causes of morbidity and mortality in diabetes are macrovasular and microvascular complications, including atherosclerosis, nephropathy, and retinopathy. As the definition of atherosclerosis as a chronic, smoldering, inflammatory disease has gained general acceptance, the attention of researchers has focused on the triggers of chronic vascular inflammation. The oxidation and other forms of modification of lipids and lipoproteins have emerged as a major pathogenic factor in atherosclerosis, with a significant interaction with the immune system. Modified lipoproteins by themselves are proinflammatory through the activation of the innate immune system as a consequence of the interaction with scavenger receptors and/or toll-like receptors expressed by a variety of cell types, including phagocytic cells and dendritic cells. A variety of modified forms of LDL (mLDL), including oxidized, malondialdehyde-modified, and Advanced Glycation End-product-modified LDL induce autoimmune responses in humans. Those modifications seem enhanced in diabetes, and the progression of atherosclerosis is accelerated in diabetic patients. The immune response to all forms of mLDL results in both activation of T cells in the arterial wall and in an autoimmune response characterized by the formation of IgG antibodies. Both arms of the immune response are believed to play a role in vascular inflammation. While the cell response is likely to activate resident macrophages, the humoral immune response results in the production of IgG antibodies that bind to specific epitopes in modified forms of LDL, generate immune complexes both intra- and extravascularly, and those complexes are able to activate the classical pathway of the complement system as well as phagocytic cells via Fc? receptors. In vitro studies suggest that the pro-inflammatory activity of immune complexes containing mLDL is several-fold higher than that of the modified LDL molecules by themselves. Clinical studies have provided significant support to the pathogenic role of immune complexes containing modified LDL in the development of atherosclerotic complications in patients with both type 1 and type 2 diabetes. At the same time, there is increasing evidence that the formation of immune complexes containing modified forms of LDL may also be involved in the pathogenesis of diabetic nephropathy and retinopathy. These are areas in which more research is needed to fully understand the pathogenic mechanisms activated by those immune complexes. Of interest is the fact that animal models have suggested the possibility of modifying the adaptive humoral immune response in ways that would result in slowing down, and perhaps prevent, the atherosclerotic process. This possibility is sufficiently alluring as to justify increased research efforts, both in animal models (including diabetic animals) and translational clinical studies. The manipulation of the T regulatory population is another area of potential translational impact, which has hardly been explored. Indeed at this point of time, what seems to be a high priority is an increased and open interchange of information among investigators, trying to reach a better general understanding and integration of knowledge generated from a variety of approaches and perspectives. This Research Topic provided an optimal platform for this open interchange of information. We encouraged interested scientists to submit mini-reviews, methods papers, review articles, perspectives and original research articles covering this topic in all its diversity to facilitate the communication of perspectives and new information between scientists interested in understanding the multiple implications of the involvement of the immune system in the pathogenesis of diabetic complications.

Genome-wide view on the physiology of vitamin D

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889193493 Year: Pages: 194 DOI: 10.3389/978-2-88919-349-3 Language: English
Publisher: Frontiers Media SA
Subject: Physiology --- Science (General)
Added to DOAB on : 2016-03-10 08:14:32
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The main physiological actions of the biologically most active metabolite of vitamin D, 1a,25-dihydroxyvitamin D3(1a,25(OH)2D3), are calcium and phosphorus uptake and transport and thereby controlling bone formation. Other emergent areas of 1a,25(OH)2D3 action are in the control of immune functions, cellular growth and differentiation. This fits both with the widespread expression of the VDR and the above described consequences of vitamin D deficiency. Transcriptome-wide analysis indicated that per cell type between 200 and 600 genes are primary targets of vitamin D. Since most of these genes respond to vitamin D in a cell-specific fashion, the total number of vitamin D targets in the human genome is far higher than 1,000. This is supported by the genome-wide view on VDR binding sites in human lymphocytes, monocytes, colon and hepatic cells. All genomic actions of 1a,25(OH)2D3 are mediated by the transcription factor vitamin D receptor (VDR) that has been the subject of intense study since the 1980’s. Thus, vitamin D signaling primarily implies the molecular actions of the VDR. In this research topic, we present in 15 chapters different perspectives on the action of vitamin D and its receptor, such as the impact of the genomewide distribution of VDR binding loci, ii) the transcriptome- and proteome-wide effects of vitamin D, iii) the role of vitamin D in health, iv) tissue-specific functions of vitamin D and v) the involvement of vitamin D in different diseases, such as infections, autoimmune diseases, diabetes and different types of cancer.

Immune-Epithelial Crosstalk in Inflammatory Bowel Diseases and Mucosal Wound Healing

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889456185 Year: Pages: 159 DOI: 10.3389/978-2-88945-618-5 Language: English
Publisher: Frontiers Media SA
Subject: Medicine (General) --- Allergy and Immunology
Added to DOAB on : 2019-01-23 14:53:43
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80% of the bodies’ immune cells are harbored within the intestine. They are only separated from 1014 microorganisms by a single layer of intestinal epithelial cells and a secreted superficial mucus layer. Therefore, the intestinal epithelial surface represents a main frontier in host defense. Providing an intact mucosal barrier is vital for the host to limit bacterial entry and spread to the circulation. This specialized localization requires dynamic responses of intestinal epithelial cells to both pathogen- and immune-derived signals. Moreover, emergency barriers are needed in the setting of epithelial damage, which allow provisional microbial control and a timely restitution of mucosal integrity. Epithelial cells constantly interact with subjacent immune cells and fibroblasts, actively directing the immune response and also shaping the luminal microbiota. Epithelial dysfunction has been appreciated in recent years as a driving element in the pathogenesis of Inflammatory Bowel Diseases (IBD). Additionally, primary immune deficiencies may manifest in the form of chronic intestinal inflammation mimicking features of IBD. Recent advances in the techniques of epithelial cell culture and the discovery of new immune cell types and cellular properties have tremendously advanced the understanding in this interesting field of research. In this research topic, we want to focus on the complex interaction of intestinal epithelial cells, luminal flora and adjacent immune cells and invite manuscripts which highlight the dynamic responses of both epithelium and immune cells under steady-state or inflammatory conditions, and envision how this may be translated to the benefit of patient-care.

How Salmonella infection can inform on mechanisms of immune function and homeostasis

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889197996 Year: Pages: 143 DOI: 10.3389/978-2-88919-799-6 Language: English
Publisher: Frontiers Media SA
Subject: Allergy and Immunology --- Medicine (General)
Added to DOAB on : 2017-02-03 17:04:57
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The use of model antigens such as haptens and ovalbumin has provided enormous insights into how immune responses develop, particularly to vaccine antigens. Furthermore, these studies are overwhelmingly performed in animals housed in clean facilities and are not known to have experienced overt clinical signs caused by infectious agents. Therefore, this is unlikely to reflect the impact more complex host-pathogen interactions can have on the host, nor the diversity in how immunity is regulated. Humans develop immune responses in the context of the periodic exposure to multiple pathogens and vaccines over a life-time. These are likely to have a long-lasting effect on who and what we are and how we respond to further antigen challenge. Therefore, studies on how infection influences immune homeostasis and how the development of responses to a pathogen reflects what is known on immune regulation will be informative on how we can translate findings from our standard models into treatments usable in humans. One organism allows us to do just this. Bacteria of the genus Salmonella are devastating human pathogens. Nevertheless, many aspects of the diseases they cause can be successfully modelled in murine systems so that the infection is either resolving or non-resolving. This has the advantage of allowing the long-term impact of infection on immune function to be assessed. We propose to welcome key workers to write about their research that examine the consequence of Salmonella infection on the host and the elements of the bacterium that contribute to this.

Systems Biology Approaches to Understanding the Cause and Treatment of Heart, Lung, Blood, and Sleep Disorders

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889192496 Year: Pages: 180 DOI: 10.3389/978-2-88919-249-6 Language: English
Publisher: Frontiers Media SA
Subject: Biotechnology --- General and Civil Engineering --- Physiology --- Science (General)
Added to DOAB on : 2015-11-16 15:44:59
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Development of powerful new high- throughput technologies for probing the transcriptome, proteome and metabolome is driving the rapid acquisition of information on the function of molecular systems. The importance of these achievements cannot be understated - they have transformed the nature of both biology and medicine. Despite this dramatic progress, one of the greatest challenges that continues to confront modern biology is to understand how behavior at the level of genome, proteome and metabolome determines physiological function at the level of cell, tissue and organ in both health and disease. Because of the inherent complexity of biological systems, the development, analysis, and validation of integrative computational models based directly on experimental data is necessary to achieve this understanding. This approach, known as systems biology, integrates computational and experimental approaches through iterative development of mathematical models and experimental validation and testing. The combination of these approaches allows for a mechanistic understanding of the function of complex biological systems in health and their dysfunction in disease. The National Heart, Lung, and Blood Institute (NHLBI) has recognized the importance of the systems biology approach for understanding normal physiology and perturbations associated with heart, lung, blood, and sleep diseases and disorders. In 2006, NHLBI announced the Exploratory Program in Systems Biology, followed in 2010 by the NHLBI Systems Biology Collaborations. The goal of these programs is to support collaborative teams of investigators in using experimental and computational strategies to integrate the component parts of biological networks and pathways into computational models that are based firmly on and validated using experimental data. These validated models are then applied to gain insights into the mechanisms of altered system function in disease, to generate novel hypotheses regarding these mechanisms that can be tested experimentally, and to then use the results of experiments to refine the models. The purpose of this Research Topic is to present the range of innovative, new approaches being developed by investigators working in areas of systems biology that couple experimental and modeling studies to understand the cause and possible treatment of heart, lung, blood and sleep diseases and disorders. This Research Topic will be of great interest to the cardiovascular research community as well as to the general community of systems biologists.

Manipulation of the host cell by viral auxiliary proteins

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889194841 Year: Pages: 118 DOI: 10.3389/978-2-88919-484-1 Language: English
Publisher: Frontiers Media SA
Subject: Microbiology --- Science (General)
Added to DOAB on : 2015-11-16 15:44:59
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Productive HIV infection requires completion of all the steps of the replication cycle, the success of which largely relying on the multiple interactions established by viral proteins with cellular partners. Indeed, cellular and viral fates are intertwined and this interplay may involve rerouting of cellular factors/pathways to the benefit of the viral life cycle. To gain a foothold into host cells, HIV has to take advantage of available cellular factories and overcome the numerous potential blocks opposed to its replication while ensuring cellular survival. Viral auxiliary proteins are a perfect paradigm to illustrate the complexity of the relationship between HIV and its host. Although these accessory proteins are mostly unnecessary for viral replication in permissive cells in vitro, they play a crucial role in regulating viral spread ex vivo in non-permissive cells and in vivo in hosts. Most accessory proteins are pleiotropic and instrumental in the counteraction of restriction factors and proteins involved in innate immune response. Several proteins of the "intrinsic" immune system that detect the presence of the assailant and initiate a subsequent immune response, as well as restriction factors that are directly devoted to arresting the replication cycle at precise steps have been characterized. Despite the numerous cellular mechanisms dedicated to preventing viral replication, HIV is able to efficiently replicate in humans. Indeed, as a master regulator of cellular machineries and processes, not only has HIV evolved strategies to avoid triggering of pattern recognition receptors, but HIV has also elaborated ways to counteract host restriction factors, thereby overcoming the hurdles that oppose efficient replication. This review collection is dedicated to the manipulation of host cells by HIV-1 and HIV-2, with a particular focus on viral accessory proteins.

Beyond the borders: The gates and fences of Neuroimmune interaction

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889192748 Year: Pages: 119 DOI: 10.3389/978-2-88919-274-8 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Neurology
Added to DOAB on : 2015-12-03 13:02:24
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Neuroimmunology is a rapidly growing emerging field at which two old sciences have converged to integrate two different types of responses into a single coherent response involving the coordinated action of both systems, neural and immune. During long time it was thought that both systems worked separately and in divergent pathways. The brain was considered an immunoprivileged site and the immune organs were deemed as independent of any neural influence and also of nervous innervation. Time has gone and has proven that the borders between both systems were merely artificial. Since the beginning of Neuroimmunology in the 1980s much work has been done to elucidate the gates and fences in neuro-immune interactions. Brain was shown to be under the continuous surveillance of the immune system, even under basal physiological conditions in the absence of any pathology. Likely, it was found a profuse nervous innervation of lymphoid organs and even of single immune cells. Gates for direct neural immune communication were found both centrally and peripherally. Centrally, the gates, but also the fences, were situated at the brain barriers, the blood-brain barrier and the blood-cerebrospinal fluid barrier, and at the circunventricular organs. Peripherally, the fences constituted the apparent diverse nature of molecules involved in neural and immune signaling; however, time proved that both system were capable of producing the same signaling molecules and also systematically responded to the molecules released by the other system. Therefore, the gates were open for direct neural-immune communication at the peripheral level. This Research Topic aimed to include original reports, reviews and technical reports regarding the description of the gates and fences in neural immune interactions. We intended to provide an extensive view of the mechanisms governing central and peripheral neural-immune interactions, and the role of the borders, the blood-neural barriers, in the regulation of the neural-immune communication.

The oral microbiome in an ecological perspective

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889195763 Year: Pages: 116 DOI: 10.3389/978-2-88919-576-3 Language: English
Publisher: Frontiers Media SA
Subject: Internal medicine --- Science (General)
Added to DOAB on : 2016-02-05 17:24:33
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The oral cavity harbors an immense diversity of microorganisms, including bacteria, fungi, archaea, protozoa and viruses. At health, oral microbial community is thought to be in a state of homeostasis, even after numerous perturbations (e.g., toothbrushing, food intake) a day. The breach in this homeostasis can occur for instance if the perturbations become too excessive (e.g., frequent carbohydrate intake leading to acidification of the community) or the host is compromised (e.g., inadequate immune response resulting in persistent inflammation of periodontal tissue). Aggressive antimicrobial therapy (e.g., antibiotics in case of periodontal disease or preventive antibiotic therapy before and after dental extractions) is commonly applied with all the negative consequences of this approach. So far little is known on the interplay between the environmental, host and microbial factors in maintaining an ecological balance. What are the prerequisites for a healthy oral ecosystem? Can we restore an unbalanced oral microbiome? How stable is the oral microbiome through time and how robust it is to external perturbations? Gaining new insights in the ecological factors sustaining oral health will lead to conceptually new therapies and preventive programs. Recent advances in high throughput technologies have brought microbiology as a science to a new era, allowing an open-ended approach instead of focusing on few opportunistic pathogens. With this topic we would like to integrate the current high-throughput ‘omics’ tools such as metagenomics, metatranscriptomics, metaproteomics or metabolomics with biochemical, physiological, genetic or clinical parameters within the oral microbial ecosystem. We aim to address questions underlying the regulation of the ecological balance in the oral cavity by including the following areas: • Ecology of oral microbiome at health • Ecology of oral microbiome under oral diseases • Ecology of oral microbiome during non-oral diseases • Shifts in the oral microbiome by therapeutic approaches (e.g., antimicrobials, replacement therapy, pre- and probiotics) • Modeling of oral ecological shifts (e.g., animal models, in vitro microcosm models) • Complex inter- and intra-kingdom interactions (e.g., bacterial-fungal-host) related to oral ecology • Environmental (e.g., diet, tobacco), host-related (e.g., immune response, saliva composition and flow) and biotic (e.g., bacterial competition) factors influencing oral ecology • Geographic variation in oral microbial ecology and diversity

Developing synaesthesia

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889195794 Year: Pages: 173 DOI: 10.3389/978-2-88919-579-4 Language: English
Publisher: Frontiers Media SA
Subject: Neurology --- Science (General)
Added to DOAB on : 2016-03-10 08:14:32
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Synaesthesia is a condition in which a stimulus elicits an additional subjective experience. For example, the letter E printed in black (the inducer) may trigger an additional colour experience as a concurrent (e.g., blue). Synaesthesia tends to run in families and thus, a genetic component is likely. However, given that the stimuli that typically induce synaesthesia are cultural artefacts, a learning component must also be involved. Moreover, there is evidence that synaesthetic experiences not only activate brain areas typically involved in processing sensory input of the concurrent modality; synaesthesia seems to cause a structural reorganisation of the brain. Attempts to train non-synaesthetes with synaesthetic associations have been successful in mimicking certain behavioural aspects and posthypnotic induction of synaesthetic experiences in non-synaesthetes has even led to the according phenomenological reports. These latter findings suggest that structural brain reorganization may not be a critical precondition, but rather a consequence of the sustained coupling of inducers and concurrents. Interestingly, synaesthetes seem to be able to easily transfer synaesthetic experiences to novel stimuli. Beyond this, certain drugs (e.g., LSD) can lead to synaesthesia-like experiences and may provide additional insights into the neurobiological basis of the condition. Furthermore, brain damage can both lead to a sudden presence of synaesthetic experiences in previously non-synaesthetic individuals and a sudden absence of synaesthesia in previously synaesthetic individuals. Moreover, enduring sensory substitution has been effective in inducing a kind of acquired synaesthesia. Besides informing us about the cognitive mechanisms of synaesthesia, synaesthesia research is relevant for more general questions, for example about consciousness such as the binding problem, about crossmodal correspondences and about how individual differences in perceiving and experiencing the world develop. Hence the aim of the current Research Topic is to provide novel insights into the development of synaesthesia both in its genuine and acquired form. We welcome novel experimental work and theoretical contributions (e.g., review and opinion articles) focussing on factors such as brain maturation, learning, training, hypnosis, drugs, sensory substitution and brain damage and their relation to the development of any form of synaesthesia.

Cellular and Phenotypic Plasticity in Cancer

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889196623 Year: Pages: 77 DOI: 10.3389/978-2-88919-662-3 Language: English
Publisher: Frontiers Media SA
Subject: Medicine (General) --- Oncology
Added to DOAB on : 2016-08-16 10:34:25
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The process of Epithelial-Mesenchymal-Transition (EMT) is known to result in a phenotype change in cells from a proliferative state to a more invasive state. EMT has been reported to drive the metastatic spread of various cancers and has also been associated with drug resistance to cytotoxics and targeted therapeutics. Recently phenotype switching akin to EMT has been reported in non-epithelial cancers such as metastatic melanoma. This process involves changes in EMT-Transcription Factors (EMT-TFs), suggesting that phenotype-switching may be common to several tumour types. It remains unclear as to whether the presence of both Epilthelial-like and Mesenchymal-like cells are a pre-requisite for phenotype switching within a tumour, how this heterogeneity is regulated, and if alteration of cell phenotype is sufficient to mediate migratory changes, or whether drivers of cell migration result in an associated phenotype switch in cancer cells. Similarly it has yet to be clarified if cells in an altered phenotype can be refractory to drug therapy or whether mediators of drug resistance induce a concurrent phenotypic change. Little is known today about the underlying genetic, epigenetic and transient changes that accompany this phenotypic switch and about the role for the tumor micro-environment in influencing it. Hence this is currently an area of speculation and keen interest in the Oncology field with wide-ranging translational implications. In this Frontiers Research Topic, we discuss our current understanding of these concepts in various cancer types including breast cancer, colorectal cancer and metastatic melanoma. This topic covers how these processes of cellular and phenotypic plasticity are regulated and how they relate to cancer initiation, progression, dormancy, metastases and response to cytotoxics or targeted therapies.

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