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This state-of-the-art reference outlines current knowledge of the structure, transcriptional regulation, and binding characteristics of vascular and leukocyte adhesion molecules and their ligands delineating the nature of adhesion molecule interactions in lung morphogenesis and repair, tumor metastasis, and experimental models of inflammatory lung injury.
This volume compares the results of investigators on the mechanisms of generation, interaction, and modulation of inflammatory cytokines and their respective cell origins and/or targets. The book, divided roughly according to cell species, advances what is currently known about the synergism of early and late mediators on resident and newly recruited target cells.
My findings have firmly established the role of ICAM-1 and LFA-1 in neutrophil recruitment into lung and have opened up unexpected directions in the role of chemokines in this process.
This book provides a comprehensive and up to date picture of the molecular mechanisms underlying acute lung injury, focusing both on the mechanisms of injury and of repair. Topics covered include the cells involved, their injurious products including pro-inflammatory cytokines, proteases and free radical species as well as the fibrotic response and its molecular regulation, the role of the immune system, airway repair and remodelling and transcription factors regulating inflammation. All the chapters are written by experts in their field and reflect the lecture given by these authors at a recent international meeting also entitled " Acute lung injury: from inflammation to repair", held as part of the ongoing Molecular Pathology Annual symposia at University College London. The meeting gathered together a wide range of scientists and clinicians all of whom are at the cutting edge of inflammation and repair as it relates to acute lung injury. It is the breadth of approach that makes the volume so useful.
Provides an overview of the structure, transcription regulation and binding characteristics of cellular adhesion molecules and their ligands in the maintenance of function, immunological reactions and inflammatory processes with organ systems. The text examines the role of adhesion molecules in biological processes such as morphogenesis, blood coagulation, tumour metastasis, bone tissue remodelling and transplant rejection.
This Research Topic assembles original contributions and reviews from an international consortium of PIs related to interactions between pro-inflammatory cytokines and ion channels during acute lung injury and chronic heart failure.
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
For the past 100 years the mainstay of therapy for rheumatoid arthritis (RA) has been aspirin or other drugs of the non-steroid anti-inflammatory group. In 1971 Vane pro posed that both the beneficial and toxic actions of these drugs was through inhibition of prostaglandin synthesis. The recent discovery that prostaglandins responsible for pain and other symptoms at inflammatory foci are synthesized by an inducible cyclooxygenase (COX-2) that is encoded by a gene distinct from that of the consti tutive enzyme (COX-I) provided a new target for therapy of RA. A drug that would selectively inhibit COX-2 would hopefully produce the symptomatic benefit provided by existing NSAIDs without the gastrointestinal and renal toxicity due to the inhibition of COX-I. Drugs selective for COX-2 are now available. Experimental studies have shown them to be effective with minimal toxicity, and in clinical trials gastric and renal toxicities are less. Highly selective COX-2 inhibitors, perhaps designed with knowledge of the crystal structures of COX-I and COX-2, are also available. Other experimental studies, including those in animals lacking effective genes for COX-lor COX-2 and in experimental carcinomas, suggest there is still much to be learned of the pathophysiological functions of these enzymes. The inflammatory response is a complex reaction involving many mediators that derive from white blood cells, endothelial cells and other tissues. Preliminary data have revealed that inhibitors of the cytokines and adhesion molecules that play a crucial role in the migration of white cells to inflammatory sites may be useful in RA.
This unique resource-the first book of its kind exclusively devoted to the subject-offers timely coverage of the cells, mechanisms, and proteins involved in allergic inflammation, emphasizing the latest advances in local cell recruitment.