The Respiratory burst and its physiological significance
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The Respiratory burst and its physiological significance
Plenum Press, c1988
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Includes bibliographies and index
内容説明・目次
内容説明
When phagocytes are exposed to a number of different stimuli, they undergo dra- matic changes in the way they process oxygen. Oxygen uptake increases markedly, frequently more than 50-fold; the phagocytes begin to produce large quantities of superoxide and hydrogen peroxide; and they immediately begin to metabolize large amounts of glucose by way of the hexose monophosphate shunt. This series of changes has become known as the respiratory burst. It was first believed that the major function of this respiratory burst was to generate powerful antibacterial agents by the partial reduction of oxygen. It is becoming apparent that the respiratory burst has much wider application, and its physiological function in many different biolog- ical areas is clear. In this volume, we have attempted to bring together the work of experts who have published extensively on the involvement of the respiratory burst in different physiological functions. In the first three chapters, Dr. Borregaard and Dr. Berton and co-workers and Dr. Roos and co-workers bring together what is known about the respiratory burst.
They present up-to-date versions of the biochemical and metabolic activities associ- ated with the burst. In Chapter 4, Dr. Styrt and Dr. Klempner discuss the respiratory burst as it affects cellular ion homeostasis. Dr. Cohen and Dr. Britigan (Chapter 5) present some interesting data on the competition between the respiratory burst and bacteria for oxygen. Dr. Dobrina and Dr.
目次
1. The Respiratory Burst: An Overview.- 1. Introduction.- 2. Biochemical Activities Associated with the Respiratory Burst.- 2.1. Origin of Electrons for the Respiratory Burst Oxidase.- 2.2. Oxygen Consumption.- 2.3. O2- Generation.- 2.4. Generation of H2O2.- 2.5. Myeloperoxidase-Mediated Reactions.- 2.6. Hydroxy 1 Radicals.- 2.7. Chemiluminescence.- 2.8. Formation of Chloramines.- 2.9. Proton Transport during the Respiratory Burst.- 2.10. Depolarization.- 3. The NADPH Oxidase.- 3.1. The NADPH Oxidase as an Electron-Transport Chain.- 3.2. Subcellular Localization of the NADPH Oxidase and Its Components...- 3.3. Activation of the NADPH Oxidase.- 4. Kinetics of the Respiratory Burst.- 5. Development of the Ability to Generate a Respiratory Burst.- 6. The Respiratory Burst in Nonphagocytic Cells.- References.- 2. The Respiratory Burst of Phagocytes.- 1. Features of the Respiratory Burst of Phagocytes.- 2. Enzymatic Basis of the Respiratory Burst.- 2.1. Major Properties of NADPH Oxidase, the O2- Generating System of Phagocytes.- 2.2. Activity of the NADPH Oxidase in Relationship to the Respiratory Burst of Intact Phagocytes.- 3. Nature of NADPH Oxidase.- 3.1. An O2- Forming Electron-Transfer Chain.- 3.2. Molecular Structure of NADPH Oxidase.- 4. Mechanisms of Activation of the Respiratory Burst.- 5. Biological Significance of the Respiratory Burst of Phagocytes.- References.- 3. The Respiratory Burst and the NADPH Oxidase of Phagocytic Leukocytes.- 1. Introduction.- 2. Intracellular Killing of Microorganisms.- 2.1. Production of Reduced Oxygen Species.- 2.2. Fusion of Granules with the Developing Phagosome.- 3. Oxidase Preparations.- 3.1. Properties of Particulate and Detergent-Treated Particulate.- Preparations.- 3.2. Properties of Solubilized Oxidase Preparations.- 4. The NADPH Oxidase System.- 4.1. Cytochrome b55B.- 4.2. A Flavoprotein.- 4.3. Ubiquinone-50.- 5. Conclusions.- References.- 4. The Respiratory Burst and Cellular Ion Homeostasis.- 1. Introduction.- 2. Ion Distribution in the Resting Neutrophil.- 2.1. Calcium.- 2.2. Hydrogen.- 2.3. Sodium, Potassium, and the Membrane Potential.- 3. Ionic Events during Activation of the Respiratory Burst.- 3.1. Calcium.- 3.2. Hydrogen.- 3.3. Sodium, Potassium, and the Membrane Potential.- 3.4. Other Ion Systems.- 4. Conclusions.- References.- 5. An Expanded View of the Phagocytic Respiratory Burst: Bacterial Competition for Oxygen and Its Stimulation by Host Factor(s).- 1. Introduction.- 1.1. Microbial Strategies to Resist Oxygen-Dependent Killing.- 2. Bacterial Competition for Oxygen.- 2.1. Limitations of Interpretation.- 3. Characterization and Purification of Serum Factor(s) That Enhance Bacterial Competition for Oxygen.- 4. Interaction with Myeloid Cells Increases Bacterial Oxygen Consumption.- 5. Summary and Conclusions.- References.- 6. The Respiratory Burst and Endothelial Cells.- 1. Introduction.- 2. Effect of Activated Neutrophils on Endothelial Cells.- 2.1. In Vitro Studies.- 2.2. Isolated Perfused Lung.- 2.3. In Vivo Studies.- 3. Mechanism(s) of Endothelial Damage by Neutrophil Activation.- 3.1. Role of the Respiratory Burst.- 3.2. Role of Neutrophil Proteases.- 3.3. Cooperation between ROI-Dependent and Protease-Dependent Mechanisms.- 4. Protective Mechanisms of Endothelial Cells against the Neutrophil Respiratory Burst.- 4.1. Inhibition of the Neutrophil Respiratory Burst by Endothelial Cells.- 4.2. Endothelial Cell Mechanisms for Of and H202 Degradation.- 5. Interactions of Neutrophils with Endothelium.- 5.1. Physiological Margination.- 5.2. Neutrophil-Endothelium Interaction during Diapedesis.- 5.3. Interaction of Neutrophils with Altered Endothelial Cells.- 5.4. Intravascular Activation of Neutrophils.- 5.5. Extravascular Activation of Neutrophils.- 6. Relationships to Human Pathology.- References.- 7. The Respiratory Burst of Eosinophils.- 1. Introduction.- 2. Studies with Eosinophils from Eosinophilic Subjects.- 3. Eosinophils from Normal Subjects versus Eosinophils from Eosinophilic Subjects.- 4. Features of the Respiratory Burst of Eosinophils.- 4.1. Induction of the Burst.- 4.2. Products of the Respiratory Burst.- 4.3. Enzymatic Basis.- 4.4. Enzymes Indirectly Related to the Respiratory Burst.- 5. Functions of the Respiratory Burst in Eosinophils.- 5.1. Microbicidal and Fungicidal Capacity.- 5.2. Helminthotoxic Activity.- 5.3. Regulation of the Activity of the Inflammatory Mediators.- 5.4. Cytotoxicity.- 6. Regulation of EPO Concentration in the Extracellular Medium.- 7. Conclusions.- References.- 8. The Respiratory Burst and Lymphocyte Function.- 1. Introduction.- 2. Characteristics of the Metabolic Burst.- 2.1. Nature of the Metabolic Burst in Phagocytic Cells.- 2.2. Generation of ROS by Lymphocytes.- 2.3. Stimuli That Induce a Metabolic Burst in Phagocytic Cells.- 3. Evidence Indicating That the ROS Produced by Phagocytic Cells May Alter the Functional Capacity of Human Lymphocytes.- 3.1. Effect of Hyperoxia on the Proliferation of Human Lymphocyte Cultures.- 3.2. Role of ROS in Radiation Damage to Lymphocytes.- 3.3. Effect of Chemical Oxidation on Lymphocyte Function.- 3.4. Effects of the ROS Generated by Enzyme Systems on the Functional Capacity of Lymphocytes in Vitro.- 3.5. Possible Differences in the Sensitivity of T and B Cells to Oxidant Damage.- 4. Evidence That the Production of ROS by Phagocytic Cells Can Alter Lymphocyte Function.- 4.1. Evidence That the Release of ROS by Phagocytic Cells May Impair the NK Activity of Lymphocytes.- 4.2. Evidence That ROS Released by Phagocytic Cells Can Alter Lymphocyte Proliferation.- 4.3. Role of the Lymphocyte in the Metabolic Burst.- 5. Summary.- References.- 9. Modulation of the Respiratory Burst by Naturally Occurring Substances.- 1. Introduction.- 2. Control of Neutrophil Respiratory Burst by Defined Biological Substances.- 3. Antiproteinases.- 4. Dialyzable Substances in Exudates of Sponge-Induced Inflammation: Polyamines.- 5. Substance P.- 6. Pneumolysin.- 7. Streptolysin O.- 8. Acid Phosphatase.- 9. Calmodulin-Binding Peptides.- 10. Platelet Activating Factor.- 11. Fructose 1,6 Diphosphate.- 12. Adenosine.- 13. Modulation of Respiratory Burst by Viral Products.- 14. Summary and Conclusions.- References.- 10. Oxidants Formed by the Respiratory Burst: Their Physiological Role and Their Involvement in the Oxidative Metabolism and Activation of Drugs, Carcinogens, and Xenobiotics.- 1. Introduction.- 2. Extracellular versus Intracellular Oxidation and Halogenation.- 3. Trapping Active Chlorine Generated by the Respiratory Burst.- 4. Physiological Role of Halogenation and Oxidation.- 4.1. Bactericidal Activity and Cell Death.- 4.2. Oxidative Inactivation of Microbial Toxins.- 4.3. Oxidative Inactivation of Methionine-Dependent Inflammation Mediators.- 4.4. Oxidative Activation of Proteases.- 4.5. Inactivation of Prostaglandins and Leukotrienes.- 4.6. Thyroxine Turnover.- 4.7. Estradiol Inactivation.- 5. Oxidative Metabolism of Drugs.- 5.1. Antithyroid Drugs.- 5.2. Oxygenation of Drugs.- 5.3. Electronic Excitation.- 6. Oxidative Activation of Carcinogens and Xenobiotics.- 6.1. Arylamines and Phenol.- 6.2. Oxygen Radicals and Singlet Oxygen.- References.- 11. Drug-Induced Agranulocytosis and Other Effects Mediated by Peroxidases during the Respiratory Burst.- 1. Metabolism of Drugs to Reactive Intermediates.- 2. Pharmacological Effects of Dapsone and Other Arylamines Mediated by Myeloperoxidase.- 3. Pharmacological and Toxic Effects of Other Drugs Metabolized by Myeloperoxidase.- 4. Possible Mechanisms of Drug-Induced Agranulocytosis.- 4.1. Direct Mechanism.- 4.2. Immune-Mediated Mechanism.- 5. Pharmacological Effects Mediated by Thyroid Peroxidase.- 6. Idiosyncratic Reactions Possibly Due to Metabolism by Monocytes.- 7. Summary.- References.- 12. The Respiratory Burst and the Metabolism of Drugs.- 1. Introduction.- 2. Characteristics of the Metabolic Burst.- 3. Relevant Studies Concerning the Metabolism of Drugs in Model Systems.- 3.1. Horseradish Peroxidase-Hydrogen Peroxide Enzyme System.- 3.2. Catalase-H202 Enzyme System.- 3.3. Arachidonic Acid Metabolism.- 3.4. The Glutathione Peroxidase Pathway.- 3.5. Microsomal Enzyme System.- 3.6. Xanthine-Xanthine Oxidase Enzyme System.- 3.7. Drug Studies in the Model System-Pulse Radiolysis.- 4. Evidence That the ROS Generated by the Myeloperoxidase System in PMN Have the Capacity to Metabolize Drugs.- 5. Evidence That Activated Granulocytes Can Oxidize and Hydroxylate Drugs.- 6. Evidence for the Metabolism of Nonsteroidal Anti-inflammatory Drugs by the Hydroxyl Radical Produced by Granulocytes.- 7. Metabolism of Drugs by Mononuclear Cells.- 8. Summary.- References.- 13. The Respiratory Burst and Carcinogenesis.- 1. Introduction.- 2. The Respiratory Burst in Phagocytes.- 3. Inflammation and Cancer.- 4. Multistep Carcinogenesis.- 4.1. Initiation.- 4.2. Promotion.- 5. Phagocyte-Generated Oxidants in Carcinogenesis.- 5.1. Oxygen-Derived Free Radicals Cause DNA Strand Breaks.- 5.2. Oxygen-Derived Free Radicals Are Mutagenic.- 5.3. Oxygen-Derived Free Radicals Cause Malignant Transformation.- 5.4. Oxygen-Derived Free Radicals Cause Nucleoside Modification.- 5.5. Oxygen-Derived Free Radicals Activate Xenobiotic Procarcinogens to Genotoxic Intermediates.- 5.6. Oxygen-Derived Free Radicals Cause Chromosomal Abnormalities.- 5.7. Oxygen-Derived Free Radicals Act as Tumor Promotors.- 6. Summary.- References.- 14. The Respiratory Burst and Mechanisms of Oxygen Radical-Mediated Tissue Injury.- 1. Introduction.- 2. Oxygen-Derived Metabolite Production by Phagocytic Cells.- 3. Host Antioxidant Defense Mechanisms.- 4. In Vitro Evidence for Phagocyte-Derived Oxygen Metabolite-Mediated Cell and Tissue Injury.- 5. In Vivo Models of Oxygen Metabolite-Mediated Tissue Injury.- 6. Summary and Conclusions.- References.- 15. The Respiratory Burst of Neutrophilic Granulocytes and Its Influence on Infected Tissues: Indirect Consequences.- 1. Reactive Species Produced Due to the Respiratory Burst.- 1.1. Triggering the Respiratory Burst.- 1.2. Reaction Pathways Originating from the Increased Oxygen Uptake by Neutrophils.- 1.3. Reactivity of the MPO-Mediated Products of the Respiratory Burst.- 2. Effects of Respiratory Burst Products on Metabolic Reactions in the Infected Tissues.- 2.1. Proteolysis.- 2.2. Changes in Nucleic Acid Metabolism.- 2.3. Degradation of Proteoglycans.- 2.4. Tentative Mechanisms of Cytotoxic and Cytolytic Activities of Neutrophils toward Target Cells.- 3. Modulation of Respiratory Burst by Its Products.- 3.1. The MPO-H2O2-C1- System as a Modulator of the Respiratory Burst.- 3.2. Influence of Cyanide on Respiratory Burst and Other Neutrophil Activities.- 4. Conclusions.- References.- 16. The Respiratory Burst and Psoriasis.- 1. Introduction.- 2. Importance of Phagocytes in Psoriasis.- 2.1. Vulgar Psoriasis.- 2.2. Pustular Psoriasis.- 3. Respiratory Burst-Related Peripheral Blood Phagocyte Function in Psoriasis.- 3.1. Chemiluminescent Response of PMN in Psoriasis.- 3.2. Chemiluminescent Response of Mononuclear Leukocytes in Psoriasis.- 3.3. Effects of Psoriatic Serum on the Respiratory Burst.- 3.4. Activity of G6PD Activity in Mononuclear Leukocytes in Psoriasis.- 4. Influence of Epidermal Cell-Culture Supernatants of Psoriatic Skin on the Respiratory Burst of Phagocytes.- 5. Effects of Psoriatic Scales on the Respiratory Burst.- 5.1. Aqueous Scale Extracts.- 5.2. Organic Extracts.- 6. Effects of PMN on Keratinocytes.- 6.1. Effect of Extracts of Scales on PMN-Mediated Cytotoxicity of Keratinocytes.- 7. Role of the Respiratory Burst in Psoriasis.- 8. Summary.- 9. Conclusion.- References.- 17. The Respiratory Burst and Diabetes Mellitus.- 1. Introduction.- 2. Alteration of the Immune System in Diabetes Mellitus.- 3. Case Studies.- 4. Reactive Oxygen Species-Generating System and the Effector Functions of Granulocytes in Diabetes Mellitus.- 5. Conclusion.- References.- 18. The Respiratory Burst of Fertilization.- 1. Introduction and Historical Perspective.- 2. The Respiratory Burst and Related Events at Fertilization.- 2.1. Initiation and Kinetics of the Respiratory Burst.- 2.2. Role of Exocytosis and Intracellular Ca2+ in the Respiratory Burst.- 2.3. Activation of NAD Kinase and the Pentose Phosphate Pathway.- 3. Peroxide Production and Fertilization Envelope Hardening.- 3.1. Assembly and Crosslinking of the Fertilization Envelope.- 3.2. Characteristics of Ovoperoxidase.- 3.3. H202 Production and Chemiluminescence.- 4. Possible Mechanisms of the Respiratory Burst.- 4.1. Lipoxygenase.- 4.2. Oxidase Activity of Ovoperoxidase.- 4.3. Other Oxidases.- 4.4. Parallels between Fertilization and Phagocytosis.- 5. Production of Activated Oxygen and Control of Toxicity.- 6. Conclusion.- References.- 19. The Respiratory Burst and Atherosclerosis.- 1. Introduction.- 2. Dual Role of Monocyte-Macrophage System in the Immune Response and in Lipid Metabolism.- 3. Dual Role of EC and SMC in the Immune Response and in Lipid.- Metabolism.- 4. Role of ROS Generation in Atherosclerotic Plaque Formation.- 5. LDL Particles as Triggers of the Respiratory Burst.- 6. Conclusion.- References.- 20. The Respiratory Burst and Aging.- 1. Introduction.- 2. General Concepts.- 2.1. Production of Free Radicals.- 2.2. Free Radical Theory of Aging.- 2.3. The Glutathione Redox Cycle.- 3. The Resting Oxidative Metabolism in the PMNL of the Elderly.- 4. The Respiratory Burst during Various Stimulations.- 4.1. Receptor Stimulation of the Respiratory Burst.- 4.2. Nonspecific Stimulation of the Respiratory Burst.- 4.3. Detoxification of Reactive Oxygen Species.- Conclusion.- References.- 21. The Respiratory Burst and the Onset of Human Labor, Preterm Labor, and Premature Rupture of the Membranes.- 1. Introduction.- 2. Phagocytosis and the Onset of Human Labor.- 2.1. Experimental Model.- 2.2. Interaction of Particulate Material and Surfactants with Amnion Cells.- 2.3. Release and Function of Amnion Phospholipase A2: Initiation of Labor at Term.- 3. Phagocytosis and Premature Rupture of the Membranes.- 3.1. Etiology of PROM.- 3.2. Role of Peroxidase in PROM.- 3.3. Surfactant and Fetal Membrane Interactions.- 4. Effect of Bacterial Growth in Fetal Membranes.- 4.1. Experimental Model.- 4.2. Nature of Effect.- 5. Summary and Concluding Remarks.- References.- 22. Tuftsin: Biochemical and Biological Aspects.- 1. Introduction.- 2. General Characteristics of Tuftsin.- 3. Phagocytosis.- 4. Motility.- 5. Toxicity of Tuftsin.- 6. Immunogenic Activity.- 7. Antibacterial Effects of Tuftsin.- 8. Antineoplastic Activity in Mice.- 9. Restoration of Disease-Depressed and Age-Depressed Functions by Tuftsin.- 10. Effect of Tuftsin on Cyclic Nucleotide Levels.- 11. Induction of Tumor Necrosis Factor by Tuftsin in Vivo and in Vitro.- 12. Reactive Oxygen Compounds.- 13. Analogues and Their Effects.- 14. Molecular Mimicry between Receptor and Antibody.- 15. Tuftsin Conformation.- 16. Synthesis of Tuftsin.- 17. Methods for Synthesis of Radioactive Tuftsin.- 18. Tuftsin Receptors.- 19. Other Studies.- 20. Tuftsin Deficiencies.- 20.1. Congenital Tuftsin Deficiency.- 20.2. Acquired Tuftsin Deficiency.- 21. Mechanism of Action.- References.
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