Dieses Fachbuch erläutert die molekularen Grundlagen von Entzündungen, spannt den Bogen zu Infektionskrankheiten und den Zusammenhang zwischen Entzündungen und chronischen Erkrankungen, behandelt abschließend den Heilungsprozess und zeigt Therapiemöglichkeiten.
The microcirculation is highly responsive to, and a vital participant in, the inflammatory response. All segments of the microvasculature (arterioles, capillaries, and venules) exhibit characteristic phenotypic changes during inflammation that appear to be directed toward enhancing the delivery of inflammatory cells to the injured/infected tissue, isolating the region from healthy tissue and the systemic circulation, and setting the stage for tissue repair and regeneration. The best characterized responses of the microcirculation to inflammation include impaired vasomotor function, reduced capillary perfusion, adhesion of leukocytes and platelets, activation of the coagulation cascade, and enhanced thrombosis, increased vascular permeability, and an increase in the rate of proliferation of blood and lymphatic vessels. A variety of cells that normally circulate in blood (leukocytes, platelets) or reside within the vessel wall (endothelial cells, pericytes) or in the perivascular space (mast cells, macrophages) are activated in response to inflammation. The activation products and chemical mediators released from these cells act through different well-characterized signaling pathways to induce the phenotypic changes in microvessel function that accompany inflammation. Drugs that target a specific microvascular response to inflammation, such as leukocyte-endothelial cell adhesion or angiogenesis, have shown promise in both the preclinical and clinical studies of inflammatory disease. Future research efforts in this area will likely identify new avenues for therapeutic intervention in inflammation. Table of Contents: Introduction / Historical Perspectives / Anatomical Considerations / Impaired Vasomotor Responses / Capillary Perfusion / Angiogenesis / Leukocyte-Endothelial Cell Adhesion / Platelet-Vessel Wall Interactions / Coagulation and Thrombosis / Endothelial Barrier Dysfunction / Epilogue / References
This book provides readers with the most up-to-date information on cutting-edge research concerning chronic inflammation. We now know that when inflammation becomes chronic, it acts as a strong disease-promoting factor in a variety of disorders including arteriosclerosis, obesity, cancer, and Alzheimer disease. Chronic inflammation is hence called as the “silent killer”; it upsets the body’s homeostatic mechanism insidiously. In spite of these developments, we know very little about the mechanism underlying chronic inflammation. Particularly, we do not know precisely what induces chronic inflammation or what promotes its prolongation in a spatiotemporal framework. Neither do we have clear knowledge about how chronic inflammation destroys various tissues or how it predisposes individuals to many different diseases. To make the situation worse, we have no effective treatment against chronic inflammation. Since 2010, two major research programs (CREST and PRESTO) aimed at clarifying the mechanisms underlying chronic inflammation were launched in Japan, and investigators of different research areas with a brilliant track record were selected by their research proposals. Subsequently they have made their best efforts to answer the conundrum concerning chronic inflammation. This book is a compendium of such research efforts. In each chapter, the CREST- or PRESTO-funded researchers summarize their original work concerning mechanisms of induction, progression, or resolution underlying chronic inflammation. The most emphasized characteristic is the molecular aspect of chronic inflammation. The book thus presents the most recent progress made in the molecular understanding of chronic inflammation.
The acute inflammatory response is the body's first system of alarm signals that are directed toward containment and elimination of microbial invaders. Uncontrolled inflammation has emerged as a pathophysiologic basis for many widely occurring diseases in the general population that were not initially known to be linked to the inflammatory response, including cardiovascular disease, asthma, arthritis, and cancer. To better manage treatment, diagnosis, and prevention of these wide-ranging diseases, multidisciplinary research efforts are underway in both academic and industry settings. This book provides an introduction to the cell types, chemical mediators, and general mechanisms of the host's first response to invasion. World-class experts from institutions around the world have written chapters for this introductory text. The text is presented as an introductory springboard for graduate students, medical scientists, and researchers from other disciplines wishing to gain an appreciation and working knowledge of current cellular and molecular mechanisms fundamental to inflammation.
Traumatic brain injury (TBI) remains a significant source of death and permanent disability, contributing to nearly one-third of all injury related deaths in the United States and exacting a profound personal and economic toll. Despite the increased resources that have recently been brought to bear to improve our understanding of TBI, the developme
Inflammation has been described as the basis of many pathologies of human disease. When one considers the updated signs of inflammation, they would be vasodilation, cell migration, and, in the case of chronic inflam- tion, cell proliferation, often with an underlying autoimmune basis. Gen- ally, inflammation may be divided into acute, chronic, and autoimmune, - though the editors believe that most, if not all, chronic states are often the result of an autoimmune response to an endogenous antigen. Thus, a proper understanding of the inflammatory basis may provide clues to new therap- tic targets not only in classical inflammatory diseases, but atherosclerosis, cancer, and ischemic heart disease as well. The lack of advances in classical inflammatory diseases, such as rh- matoid arthritis, may in part arise from a failure to classify the disease into different forms. That different forms exist is exemplified in patients with d- fering responses to existing antiinflammatory drugs, ranging from nonresponders to very positive responders for a particular nonsteroidal an- inflammatory drug (NSAID). Though researchers have progressively unr- eled the mechanisms, the story is far from complete. It should also be noted that the inflammatory response is part of the innate immune response, or to use John Hunter’s words in 1795, “inflammation is a salutary response.” That may be applied in particular to the defensive response to invading micro- ganisms.
This volume examines in detail the role of chronic inflammatory processes in the development of several types of cancer. Leading experts describe the latest results of molecular and cellular research on infection, cancer-related inflammation and tumorigenesis. Further, the clinical significance of these findings in preventing cancer progression and approaches to treating the diseases are discussed. Individual chapters cover cancer of the lung, colon, breast, brain, head and neck, pancreas, prostate, bladder, kidney, liver, cervix and skin as well as gastric cancer, sarcoma, lymphoma, leukemia and multiple myeloma.
The book describes how the balance between pro- and anti-inflammatory molecules is related to health and disease. It is suggested that many diseases are initiated and their progress is influenced by inflammatory molecules and a decrease in the production and/or action of anti-inflammatory molecules and this imbalance between pro- and anti-inflammatory molecules seems to have been initiated in the perinatal period. This implies that strategies to prevent and manage various adult diseases should start in the perinatal period. An alteration in the metaolism of essential fatty acids and their anti-inflammatory molecules such as lipoxins, resolvins, protecitns, maresins and nitrolipids seems to play a major role in the pathobiology of several adult diseases. Based on these concepts, novel therapeutic approaches in the management of insulin resistance, obesity, type 2 diabetes mellitus, metabolic syndrome, cancer, lupus, rheumatoid arthritis and other auto-immune diseases are presented. Based on all these evidences, a unified concept that several adult diseases are due to an alteration in the balance between pro- and anti-inflammatory molecules is discussed and novel methods of their management are presented.
This book covers the physiological processes relevant to inflammation. It centers on the recruitment of leukocytes to sites of injury and infection, their function in the tissue and the eventual resolution of inflammation.