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Plasticity Of Monocytes Macrophages Phenotypic Changes During Disease Progression


Plasticity Of Monocytes Macrophages Phenotypic Changes During Disease Progression
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Plasticity Of Monocytes Macrophages Phenotypic Changes During Disease Progression


Plasticity Of Monocytes Macrophages Phenotypic Changes During Disease Progression
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Author : Ruoxi Yuan
language : en
Publisher: Frontiers Media SA
Release Date : 2023-12-07

Plasticity Of Monocytes Macrophages Phenotypic Changes During Disease Progression written by Ruoxi Yuan and has been published by Frontiers Media SA this book supported file pdf, txt, epub, kindle and other format this book has been release on 2023-12-07 with Medical categories.


Macrophage is a key component of innate immunity that exhibit extensive plasticity and heterogeneity. They are present in virtually every organ of the body and can be replenished by circulating monocytes following insults. Originally macrophages were divided into two major phenotypes: pro-inflammatory M1, which is initiated by TNF-α, INF-γ, and bacterial components such as lipopolysaccharide (LPS), and anti-inflammatory M2, which is activated through stimulation of IL-4, IL-10, and IL-13. However, segregation into two distinct phenotypes is a marked simplification of the in vivo reality and it is now widely accepted that macrophage phenotype is plastic and determined by highly complex microenvironments, and therefore likely more accurately considered as a spectrum of possible forms of activation. Numerous studies have documented flexibility in their programming, with macrophages switching from one functional phenotype to another in response to the variable microenvironmental signals of the local milieu. Various macrophage populations exist that play distinct and non-redundant roles in fibrosis, tissue repair, and regeneration. For instance, in a general wound healing process, embryo-derived tissue-resident macrophages are rapidly replaced by monocytes after the initial injury. These monocyte-derived macrophages play an active role in the early initiation of acute inflammation. As early as 24–72 h upon tissue injury, macrophage function changes toward an anti-inflammatory phenotype that promotes cell proliferation and tissue remodeling. Upon resolution of inflammation, steady-state self-maintenance of macrophages is also recovered. The wound microenvironment has a predominant role in the behavior and functionality of cells. Both mouse and human diabetic wound preferably induce persistent proinflammatory macrophage polarization that contributes to chronic, non-healing wounds. Contrastingly, prolonged activation of M2 macrophages can also lead to excessive wound healing and ultimately fibrosis. In the context of cancer, anti-inflammatory macrophages have been associated with tumor progression and immunosuppression, thereby negatively affecting the prognosis of patients. On the other hand, studies also showed that the phenotypical changes of macrophages are also accompanied by changes in glycolysis and mitochondrial-related genes as well. Classically activated, proinflammatory M1 macrophages depend to a large extent on glycolysis and produce lactate as the tricarboxylic acid cycle is blocked at two steps. Alternatively, activated M2 macrophages prefer β-oxidation and oxidative phosphorylation to synthesize ATP. However, the number and diversity of signals and the magnitude of the response required to switch macrophages into a pro or anti-inflammatory state remain unclear. A number of techniques have been developed over the years to identify and visualize cell populations, uncover regulatory relationships between genes, and track the trajectories of distinct cell lineages in development. The identification of mechanisms and molecules associated with macrophage plasticity and polarized activation provides a basis for macrophage-centered diagnostic and therapeutic strategies. Understanding and being able to controllable promote the desired macrophage phenotypes could have a significant impact on a wide range of diseases.



Muscle Regeneration


Muscle Regeneration
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Author : Alexander Mauro
language : en
Publisher: Raven Press (ID)
Release Date : 1979

Muscle Regeneration written by Alexander Mauro and has been published by Raven Press (ID) this book supported file pdf, txt, epub, kindle and other format this book has been release on 1979 with Medical categories.




Tissue Repair And Fibrosis


Tissue Repair And Fibrosis
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Author : Alexis Desmouliere
language : en
Publisher: Springer Science & Business Media
Release Date : 2012-12-06

Tissue Repair And Fibrosis written by Alexis Desmouliere and has been published by Springer Science & Business Media this book supported file pdf, txt, epub, kindle and other format this book has been release on 2012-12-06 with Medical categories.


With contributions by numerous experts



Human Monocytes


Human Monocytes
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Author : Marek Zembala
language : en
Publisher:
Release Date : 1989

Human Monocytes written by Marek Zembala and has been published by this book supported file pdf, txt, epub, kindle and other format this book has been release on 1989 with Medical categories.


Monocytes represent one of the major types of white blood cells in man which prevent infection by ingesting and killing invading pathogens and by releasing factors which stimulate and regulate lymphocytes. Monocytes "purify" the blood, removing immune complexes, mediating inflammatory responses, and initiating tissue repair. Human Monocytes represents an up-to-date, definitive account of this important cell. It covers the cells biochemical, immunological, and inflammatory functionsand its role in many diseases, including asthma, atherosclerosis, rheumatoid arthritis, and AIDS.



The M2 Macrophage


The M2 Macrophage
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Author : Tamás Röszer
language : en
Publisher: Springer Nature
Release Date : 2020-08-03

The M2 Macrophage written by Tamás Röszer and has been published by Springer Nature this book supported file pdf, txt, epub, kindle and other format this book has been release on 2020-08-03 with Medical categories.


Macrophages are core components of the innate immune system. Once activated, they may have either pro- or anti-inflammatory effects that include pathogen killing, safe disposal of apoptotic cells or tissue renewal. The activation state of macrophages is conceptualized by the so-called M1/M2 model of polarization. M2 macrophages are not simply antagonists of M1 macrophages; rather, they represent a network of tissue resident macrophages with roles in tissue development and organ homeostasis. M2 macrophages govern functions at the interfaces of immunity, tissue development and turnover, metabolism, and endocrine signaling. Dysfunction in M2 macrophages can ruin the healthy interplay between the immune system and metabolic processes, and lead to diseases such as insulin resistance, metabolic syndrome, and type 1 and 2 diabetes mellitus. Furthermore, M2 macrophages are essential for healthy tissue development and immunological self-tolerance. Worryingly, these functions of M2 macrophages can also be disrupted, resulting in tumor growth and autoimmunity. This book comprehensively discusses the biology of M2 macrophages, summarizes the current state of knowledge, and highlights key questions that remain unanswered.



M1 M2 Macrophages The Arginine Fork In The Road To Health And Disease


M1 M2 Macrophages The Arginine Fork In The Road To Health And Disease
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Author : Charles Dudley Mills
language : en
Publisher: Frontiers Media SA
Release Date : 2015-03-23

M1 M2 Macrophages The Arginine Fork In The Road To Health And Disease written by Charles Dudley Mills and has been published by Frontiers Media SA this book supported file pdf, txt, epub, kindle and other format this book has been release on 2015-03-23 with Immunologic diseases categories.


Macrophages have unique and diverse functions necessary for survival. And, in humans (and other species), they are the most abundant leukocytes in tissues. The Innate functions of macrophages that are best known are their unusual ability to either “Kill” or “Repair”. Since killing is a destructive process and repair is a constructive process, it was stupefying how one cell could exhibit these 2 polar – opposite functions. However, in the late 1980’s, it was shown that macrophages have a unique ability to enzymatically metabolize Arginine to Nitric Oxide (NO, a gaseous non – specific killer molecule) or to Ornithine (a precursor of polyamines and collagen for repair). The dual Arginine metabolic capacity of macrophages provided a functional explanation for their ability to kill or repair. Macrophages predominantly producing NO are called M1 and those producing Ornithine are called M2. M1 and M2 – dominant responses occur in lower vertebrates, and in T cell deficient vertebrates being directly driven by Damage and Pathogen Associated Molecular Patterns (DAMP and PAMP). Thus, M1 and M2 are Innate responses that protect the host without Adaptive Immunity. In turn, M1/M2 is supplanting previous models in which T cells were necessary to “activate” or “alternatively activate” macrophages (the Th1/Th2 paradigm). M1 and M2 macrophages were named such because of the additional key findings that these macrophages stimulate Th1 and Th2 – like responses, respectively. So, in addition to their unique ability to kill or repair, macrophages also govern Adaptive Immunity. All of the foregoing would be less important if M1 or M2 – dominant responses were not observed in disease. But, they are. The best example to date is the predominance of M2 macrophages in human tumors where they act like wound repair macrophages and actively promote growth. More generally, humans have become M2 – dominant because sanitation, antibiotics and vaccines have lessened M1 responses. And, M2 dominance seems the cause of ever - increasing allergies in developed countries. Obesity represents a new and different circumstance. Surfeit energy (e.g., lipoproteins) causes monocytes to become M1 dominant in the vessel walls causing plaques. Because M1 or M2 dominant responses are clearly causative in many modern diseases, there is great potential in developing the means to selectively stimulate (or inhibit) either M1 or M2 responses to kill or repair, or to stimulate Th1 or Th2 responses, depending on the circumstance. The contributions here are meant to describe diseases of M1 or M2 dominance, and promising new methodologies to modulate the fungible metabolic machinery of macrophages for better health.



Macrophage Plasticity In Sterile And Pathogen Induced Inflammation


Macrophage Plasticity In Sterile And Pathogen Induced Inflammation
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Author : Ioannis Kourtzelis
language : en
Publisher: Frontiers Media SA
Release Date : 2022-02-04

Macrophage Plasticity In Sterile And Pathogen Induced Inflammation written by Ioannis Kourtzelis and has been published by Frontiers Media SA this book supported file pdf, txt, epub, kindle and other format this book has been release on 2022-02-04 with Medical categories.




Obesity


Obesity
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Author : Debasis Bagchi
language : en
Publisher: CRC Press
Release Date : 2007-03-07

Obesity written by Debasis Bagchi and has been published by CRC Press this book supported file pdf, txt, epub, kindle and other format this book has been release on 2007-03-07 with Medical categories.


The obesity epidemic has spawned an unlimited array of quick-fix, rapid weight loss plans and unproven pharmaceuticals. Dangerous side effects and rebound weight gain has made the cure seem worse than the syndrome itself and left people uncertain where to turn. The only way to safely deal with the global obesity problem is to develop strategic ther



Fibrosis In Disease


Fibrosis In Disease
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Author : Monte S. Willis
language : en
Publisher: Springer
Release Date : 2018-11-10

Fibrosis In Disease written by Monte S. Willis and has been published by Springer this book supported file pdf, txt, epub, kindle and other format this book has been release on 2018-11-10 with Medical categories.


Fibroproliferative diseases are a broad spectrum of entities from organ-specific involvement (e.g., pulmonary, heart, liver, and kidney fibrosis) to multi-system diseases such as systemic sclerosis and sclerodermatous graft vs. host disease. These diseases also encompass pathophysiologies not readily recognizably related, such as macular degeneration and cancer metastasis. Fibroproliferative diseases are a leading cause of morbidity and mortality and can affect all tissues and organ systems. Remarkable progress in elucidating the pathogenesis of these common diseases with fibrotic components, including the critical roles of myofibroblasts and the molecular mechanisms driving the transcriptional activation involved in the induction of fibrosis. As the importance of these processes is realized in the long-term recovery and treatment of diseases, effective anti-fibrotic therapies targeting the underlying ongoing disease processes are lacking. The complexity of discovering and applying therapies to fibroproliferative disease may be due to the diversity of the systems the pathogenesis of disease itself involves. By nature, fibroproliferative diseases are interdisciplinary, involving multiple cell types (organ-specific epithelial cells), immune cells, endothelial cells, and fibroblasts. Bone marrow, cytokines, and organ-specific pathologies further speckle both the clinical and scientific disciplines in such a way that communication is often limited to the clinical or scientific tribes we live in, despite the greatest access to information known to man available today. Therefore, the primary focus of this text is to bring together authors from a diversity of both clinical, scientific, and therapeutic backgrounds for readers to more fully appreciate that fantastic platform that is available to build upon to lessen the isolation of the clinical and scientific disciplines. With advances in the discovery of pre-clinical therapeutic targets (at least 20+ to date) involving TGF-beta (and other cytokines), transcription factors, and downstream kinases, it’s important to both recognize the broader impact and potential opportunities that exist even today. This book will serve as a state-of-the-art resource for physicians and translational medical researchers alike who are interested in the rapidly evolving field of fibroproliferative diseases. The book will provide new insight into the fundamental mechanisms of classic fibrotic pathophysiologic processes like myocardial infarction, idiopathic pulmonary fibrosis, chronic kidney disease, wound healing, and systemic sclerosis. It will also highlight the many new areas of therapeutic investigation currently underway. Lastly, we will touch upon newly emerging fields investigating the role of fibrosis in macular degeneration and cancer metastasis. The chapters will be written by established experts in their fields, including clinicians (cardiologists, cardiovascular surgeons, pathologists, and general practitioners) and translational biomedical researchers in a wide range of disciplines. However, the material will certainly have a broader audience including medical residents, fellows, and general practitioners as well as M.D. or Ph.D. post-doctoral research fellows. While comprehensive, we'll attempt to present the material in a manner that simplifies the complex pathophysiologic mechanisms that underlie common fibroproliferative diseases while making it appealing to a broad audience.



Control Of Regulatory T Cell Stability Plasticity And Function In Health And Disease


Control Of Regulatory T Cell Stability Plasticity And Function In Health And Disease
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Author : Margarita Dominguez-Villar
language : en
Publisher: Frontiers Media SA
Release Date : 2021-03-08

Control Of Regulatory T Cell Stability Plasticity And Function In Health And Disease written by Margarita Dominguez-Villar and has been published by Frontiers Media SA this book supported file pdf, txt, epub, kindle and other format this book has been release on 2021-03-08 with Medical categories.