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An accompanying volume (Volume 6) in this series presents strategies of cellular invasion from the viewpoint of the microbe. This filed of study is growing rapidly after a somewhat slow start over recent decades. This collection of invited chapters attempts to reflect current research, and brings together cell biologists, microbiologists and immunologists with disparate interests. However, there is a certain unity, even repetition of key themes, hopefully like a symphony rather than a boring catalogue. It will be evident that editorial bias favors intracellular paratism and medically impor
Phagocytosis. --- Phagocytes. --- Macrophages.
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Macrophages were first discovered in 1882 when Elia Metchnikoff recognized them as important phagocytic cells that can engulf any foreign material, including fungal spores. This discovery has proved to be a milestone in establishing the field of innate immunity. Macrophages are still ruling the area after 140 years of their discovery. This book explores the diverse role of macrophages in vertebrate immunity, parasitic, bacterial, and viral infections, regeneration, inflammation, and neurological diseases.
Macrophages --- Activation. --- Research --- Methodology.
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Macrophages. --- Natural immunity. --- Macrophages --- Immunité naturelle --- Natural immunity --- Immunité naturelle
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Mononuclear Phagocyte System. --- Reticulo-endothelial system. --- Macrophages. --- Macrophages --- Human histology. Human cytology --- Human physiology
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Macrophages --- Phagocytosis --- Macrophages. --- Phagocytosis. --- Histiocytes --- Mononuclear phagocytes --- Antigen presenting cells --- Connective tissue cells --- Killer cells --- Phagocytes --- Reticulo-endothelial system
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This eBook is a collection of articles from a Frontiers Research Topic. Frontiers Research Topics are very popular trademarks of the Frontiers Journals Series: they are collections of at least ten articles, all centered on a particular subject. With their unique mix of varied contributions from Original Research to Review Articles, Frontiers Research Topics unify the most influential researchers, the latest key findings and historical advances in a hot research area! Find out more on how to host your own Frontiers Research Topic or contribute to one as an author by contacting the Frontiers Editorial Office: frontiersin.org/about/contact
Medicine --- Immunology --- phagocytosis --- phagosome --- CR3 --- necrotic debris --- efferocytosis --- macrophages --- microglia --- opsonins
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It is by now widely recognized that atherosclerosis – with its burden of consequences in cerebro- and cardiovascular diseases – is just a chronic inflammatory process of the arterial wall. A very peculiar, complex and as yet still poorly understood process, upon which hundreds of scientists from several different fields are continuously concentrating their investigative efforts in search of possible leads to therapeutic approaches. Initiation of the disease is given by deposition of lipid in the intimal layers, resulting in endothelial activation and infiltration of blood-derived mononuclear cells. These mature into macrophages, become activated, express scavenger receptors such as SR-A and CD36 and ingest the oxidized lipoprotein accumulating in the lesion. Macrophages thus represent an obvious target for intervention, as they play a crucial role in the progression of the atherosclerotic inflammation. Studies have shown that hypercholesterolaemia can increase monocyte mobilisation from bone marrow into the circulation, and several chemokines and their receptors are involved in the recruitment of blood borne monocytes into the arterial wall. Monocyte-derived macrophages are capable of sustaining their local proliferation, but resident macrophages possibly also participate in progression of the disease. Remarkably, smooth muscle cells can acquire macrophage-like features during atherogenesis, including the ability to uptake lipid, thus becoming a significant proportion of the CD68+ so called ‘foam cells’. Lipid-laden macrophages induce extracellular matrix degradation, while lipid uptake eventually causes their death with formation of a necrotic core. The efficiency in clearance of dead cells by phagocytes (efferocytosis), can also be considered as a determinant of plaque vulnerability. An important feature of macrophages is their great plasticity and functional diversity in response to signals from the plaque microenvironment. Several such ‘signals’ (cholesterol, oxidative stress, hypoxia, cytokines…) can in fact modulate cell differentiation at transcriptional and epigenetic levels, thus altering the balance between the effector vs. reparative functions of macrophages. A whole gamut of specific subsets are thus originated, which appear to be simultaneously present in lesions with proportions that vary according to their location, the disease stage, and the presence of additional cell types such as e.g. dendritic cells. The result is a multiplicity of potential pharmacological targets, representing a major obstacle for the devisement of therapeutic strategies. Experimental approaches have been attempted in diverse directions: e.g. modulating the macrophage phenotype to an anti-inflammatory and resolving state, or blocking pro-inflammatory cytokines that macrophages produce, or alternatively enhancing efferocytosis in order to favour the resolution of inflammation and stabilization of plaques. Blocking monocyte recruitment was proposed in order to hinder the initial steps of atherogenesis. Other treatments were aimed to inhibiting local proliferation of pro-inflammatory macrophages. Specific targeting of macrophages has however to date not yet provided significant, translational results. The present Research Topic collects articles to help unravel the complexity of macrophage behaviour in atherosclerosis and identify innovative pharmacological approaches.
Science: general issues --- Pharmacology --- monocytes/macrophages --- inflammation --- foam cell formation --- smooth muscle cells --- atherosclerosis progression
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Streptococcus pneumoniae has been for decades the number one bacterial killer of children in the world. Although vaccination with pneumococcal vaccines [PCV7, PCV10, and PCV13 (children) or PPSV23 (adults)] has helped decrease the burden of pneumococcal disease (PD), mortality remains high. Therefore, pathogenesis studies are still key toward our understanding of PD and its control. The introduction of pneumococcal vaccines has also created a niche for vaccine-escape clones. Moreover, the rise of multi-drug resistant clones around the world has also posed a serious threat in recent years. The proposed special issue of Frontiers in Cellular and Infection Microbiology highlights many of the recent advances that have been made in pneumococcal pathogenesis, colonization and antibiotic resistance by groups in Latino America, Europe, and the USA.
pathogenesis --- macrophages --- co-infection --- gene regulation --- biofilm --- drug resistance --- microbial --- Streptococcus pneumoniae
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This eBook is a collection of articles from a Frontiers Research Topic. Frontiers Research Topics are very popular trademarks of the Frontiers Journals Series: they are collections of at least ten articles, all centered on a particular subject. With their unique mix of varied contributions from Original Research to Review Articles, Frontiers Research Topics unify the most influential researchers, the latest key findings and historical advances in a hot research area! Find out more on how to host your own Frontiers Research Topic or contribute to one as an author by contacting the Frontiers Editorial Office: frontiersin.org/about/contact
Medicine --- Immunology --- Metabolism --- Glycolysis --- oxidative phosphrylation --- Tumor Microenvironment --- immune cells --- T cells --- Macrophages --- Endothelial Cells
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