The Reticuloendothelial System

IV. Regulation and Macrophage Secretions.- 1. Endocrinelike Activities of the RES: An Overview.- 1. Introduction.- 2. Macrophage Factors Regulating Lymphocyte Functions.- 2.1. Interleukin 1 (Lymphocyte-Activating Factor).- 2.2. Thymic Maturation Factor.- 2.3. Genetically Related Factor.- 2.4. Interferon.- 2.5. Glucocorticoid Response-Modifying Factor.- 2.6. Prostaglandins and Oxygen Metabolites.- 3. Macrophage Factors Regulating Nonlymphoid Cells.- 3.1. Leukocytic Endogenous Mediator (Endogenous Pyrogen).- 3.2. Synovial Cell- and Chondrocyte-Stimulating Factors.- 3.3. Serum Amyloid A-Inducing Factor.- 3.4. Fibroblast-Activating Factor and Corneal Cell Factor.- 3.5. Glucocorticoid-Antagonizing Factor and Macrophage Insulinlike Activity.- 4. Macrophage Factors Regulating Cells of the RES.- 4.1. Colony-Stimulating Factor and Factor Inducing Monocytopoiesis.- 4.2. Interferon.- 4.3. Prostaglandins.- 5. Concluding Remarks.- References.- 2. Regulation of Complement Synthesis in Mononuclear Phagocytes.- 1. Introduction.- 2. Historical.- 3. Systems Used to Assay for Synthesis of Complement Proteins.- 4. Regulation of Complement Synthesis by Mononuclear Phagocytes.- 4.1. Posttranslational Modification.- 4.2. Effect of Agents Used to Induce a Peritoneal Exudate.- 4.3. Percentage of Mononuclear Phagocytes That Synthesize Complement.- 4.4. Effect of Phagocytosis.- 4.5. Kinetics of Complement Production by Human Peripheral Blood Monocytes and the Effect of Lymphokine on the Rate and Extent of Production.- 4.6. Effect of Culture Surfaces on Capacity of Macrophages and Monocytes to Produce Complement.- 4.7. Effect of Cortisone and Cyclophosphamide.- 4.8. Alteration of Complement Synthesis during Disease States.- 4.9. Miscellaneous.- References.- 3. The Synthesis of Arachidonic Acid Oxygenation Products by Macrophages.- 1. Introduction.- 2. Synthesis of Arachidonic Acid Oxygenation Products via the Cyclooxygenase Pathway in Mononuclear Phagocytes.- 2.1. Mouse Peritoneal Macrophages.- 2.2. Regulation of Prostaglandin Synthesis by Mouse Peritoneal Macrophages.- 2.3. The Phospholipases of Mouse Peritoneal Macrophages.- 2.4. Prostaglandin Synthesis by Mouse Peritoneal Macrophages Is Dependent on RNA and Protein Synthesis.- 2.5. Variations in the Nature and Extent of Cyclooxygenase Product Formation by Resident and Elicited Mouse Peritoneal Macrophages and Mononuclear Phagocytes from Other Sources in the Mouse.- 2.6. The Synthesis of Products of the Cyclooxygenase Pathway by Human Peripheral Blood Monocytes.- 3. Synthesis of Lipoxygenase Pathway Products by Macrophages.- 4. Concluding Remarks.- References.- 4. Lysosomal Hydrolases.- 1. Introduction.- 2. The Monocyte Granules.- 3. From Monocytes to Macrophages.- 4. The Lysosomal Apparatus of Macrophages.- 4.1. Introduction.- 4.2. Subcellular Fractionation of Alveolar Macrophages.- 4.3. Subcellular Fractionation of Peritoneal Macrophages and Bone Marrow-Derived Macrophages.- 4.4. Ultrastructure of Alveolar and Peritoneal Macrophages.- 5. Lysosomal Enzyme Levels in Differentiating Macrophages.- 6. The Release of Lysosomal Enzymes from Macrophages.- 6.1. Release into Phagocytic Vacuoles.- 6.2. Release by Secretion.- 7. Stimulus-Induced Secretion of Lysosomal Enzymes.- 7.1. Induction by Phagocytosis.- 7.2. Induction by Nonphagocytic Stimuli.- 7.3. The Mechanism of Lysosomal Enzyme Secretion by Macrophages.- References.- 5. Macrophage Neutral Proteinases: Nature, Regulation, and Role.- 1. Introduction.- 2. Nature of Macrophage Neutral Proteinases.- 2.1. Background.- 2.2. General Aspects.- 2.3. Plasminogen Activator.- 3. Localization of Macrophage Neutral Proteinases.- 3.1. General Considerations.- 3.2. Plasminogen Activator.- 4. Regulation of Neutral Proteinase Activities in Macrophages.- 4.1. General Considerations.- 4.2. Inflammation.- 4.3. Endotoxin.- 4.4. Surface Receptors and Endocytosis.- 4.5. Immune Regulation.- 4.6. Colony-Stimulating Factors.- 4.7. Hormonal and Pharmacological Control.- 4.8. Proteinases, Peptides, and Antiproteinases.- 5. Role of Proteinase in Macrophage Function.- 5.1. General Comments.- 5.2. Fibrinolysis.- 5.3. Activation of Plasma Proteinase Cascades.- 5.4. Catabolism of Connective Tissue and Other Proteins.- 5.5. Cell Surfaces, Adherence, and Endocytosis.- 5.6. Macrophage Activation.- 5.7. Macrophage Proliferation.- 5.4. Prostaglandin Synthesis.- 6. Addendum.- 7. Conclusion.- References.- 6. Interferon and Macrophages.- 1. Introduction.- 2. Macrophages as Producers of Interferon.- 3. Inducers for Macrophage Interferon Production.- 4. Importance of the Degree of Maturation of the Macrophage for Interferon Production.- 5. Relationships of Macrophage Interferon to Other Macrophage Products.- 6. Kinetics and Process of Interferon Induction in Macrophages.- 7. The Macrophage as an Accessory Cell for Interferon Production.- 8. The Role of Macrophages for in Vivo Interferon Production.- 9. Effects of Interferon on Macrophages.- 10. Concluding Comments.- References.- 7. Leukocytic Endogenous Mediator in Nonspecific Host Defenses.- 1. Introduction.- 2. Isolation of LEM and Its Physiochemical Properties.- 2.1. Isolation and Purification.- 2.2. Physiochemical Properties.- 2.3. Differentiation from Bacterial Endotoxin.- 3. Comparison of LEM to IL-1 and EP.- 4. Cells and Conditions Involved in Production and Release of LEM.- 4.1. Cells Which Produce LEM.- 4.2. Activation of Cells to Release LEM.- 4.3. Synthesis and Release Conditions.- 5. Biological Activities of LEM.- 5.1. Neutrophilia and Granulopoiesis.- 5.2. Zinc Metabolism.- 5.3. Iron Metabolism.- 5.4. Copper Metabolism.- 5.5. Acute-Phase Proteins.- 5.6. Protection against Bacterial Infection.- 5.7. Other Biological Activities.- 6. Summary.- References.- V. Clinical Physiology of the RES.- 8. Evaluation of RES Clearances in Man.- 1. Introduction.- 2. Methods Available for Evaluation of RES Clearances in Man.- 2.1. Detection and Measurement of Spillover of Endogenous Substances.- 2.2. Clearance of Exogenous Test Particles Injected Intravenously.- 2.3. Investigation of Stages in RES Clearances.- 3. Conclusions.- References.- 9. RES Function in Experimental and Human Liver Disease.- 1. Introduction.- 2. RES Function in Experimental Liver Disease Related to Human Abnormalities.- 2.1. Acute Liver Disease.- 2.2. Chronic Liver Disease.- 2.3. Summary: Influence of Experimental Liver Disease on RES Function.- 3. RES Function in Human Liver Disease.- 3.1. RES Function and Acute Liver Disease.- 3.2. RES Function and Acute Alcoholic Liver Disease.- 3.3. RES Function and Chronic Liver Disease.- 4. Summary and Perspective.- References.- 10. Regional Phagocytosis in Man.- 1. Introduction.- 2. The Liver.- 2.1. Radiopharmaceuticals.- 2.2. The Normal Liver.- 2.3. The Liver Scan in Disease.- 3. The Spleen.- 3.1. Radiopharmaceuticals.- 3.2. The Normal Spleen.- 3.3. The Spleen Scan in Disease.- 4. Bone Marrow.- 4.1. Radiopharmaceuticals.- 4.2. The Normal Bone Marrow.- 4.3. Bone Marrow Scans in Disease.- 5. The Lymph System.- 5.1. Radiopharmaceuticals.- 5.2. The Normal Lymph Node.- 5.3. Lymph Node Imaging in Disease.- References.- 11. Inflammatory Cell Dynamics in Man.- 1. Definitions.- 1.1. Acute Inflammation Due to Trauma.- 1.2. Acute Immune Response in Inflammation.- 1.3. The Lymphocyte in Man.- 1.4. The Monocyte in Man.- 2. Observations on the Cell-Mediated Immune Response and the Sequence of Leukocytic Migrations.- 2.1. The Acute Immune Response in Inflammation in Man.- 2.2. Phagocytic Activity of Transforming Lymphocytes in Inflammation in Man.- 3. Critique.- 3.1. Immunological Dissection of Leukocytic Inflammatory Responses in Skin Windows in Man.- 3.2. Leukocytic Responses to Abnormal Inflammatory Stimuli.- 3.3. Abnormal Leukocytic Responses to Normal Inflammatory Stimuli.- 4. Discussion.- 4.1. Neutrophilic Functions.- 4.2. The Monocyte of Man in Inflammation.- 4.3. The Lymphocyte in Man: Amplification and Dynamism in Inflammation.- 5. Summary.- References.- 12. Fibronectin and Reticuloendothelial Clearance of Blood-Borne Particles: Clinical Studies in Septic Shock.- 1. Introduction.- 2. Opsonic Glycoprotein (Plasma Fibronectin) Depletion and Particulate Removal.- 3. Reticuloendothelial Systemic Defense and Traumatic Injury.- 4. Organ Failure in Shock and RE Function.- 5. Opsonic ?2-SB Glycoprotein and Plasma Fibronectin.- 6. Cell Surface Fibronectin as Related to Plasma Fibronectin.- 7. Cryoprecipitate Infusion and Organ Function in Septic Injured Patients.- 8. Microvascular Fluid and Solute Exchange and Fibronectin.- 9. Antibacterial Defense by Phagocytosis and Fibronectin.- 10. Conclusions and Significance.- References.- VI. Integrative Functions of the RES.- 13. Physiology and Pathophysiology of Pulmonary Macrophages.- 1. Introduction.- 2. Types of Pulmonary Macrophages.- 3. Origin of Pulmonary Macrophages.- 4. Fate of Pulmonary Macrophages.- 5. Quantitation and Harvesting Techniques.- 6. Role of Pulmonary Macrophages.- 7. Pathophysiology of Pulmonary Macrophages.- 8. Conclusion.- References.- 14. Temperature Regulation and Fever.- 1. Introduction.- 2. Basic Thermal Physiology.- 3. Neuronal Integration during Fever.- 3.1. General Consideration.- 3.2. The CNS and Fever.- 4. Leukocyte Pyrogen.- 4.1. Characteristics.- 4.2. Nonpyrogenic Effects of LP.- 4.3. Immune Fever.- 4.4. LP as a Monokine.- 5. Cell Sources of LP.- 5.1. Historical Background.- 5.2. Characteristics of LP Release from Mononuclear Phagocytes.- 5.3. Kupffer Cells.- 6. Summary.- References.- 15. Microcirculatory Regulation and Dysfunction: Relationship to RES Function and Resistance to Shock and Trauma.- 1. Introduction.- 2. Microcirculation.- 2.1. Architecture, Ultrastructure, and Density of Adrenergic Innervation.- 2.2. Function and Regulation.- 2.3. Criteria for a Substance to Be Classified a Local Regulator of Blood Flow.- 2.4. Important Candidates for Regulators of Blood Flow.- 3. Microcirculatory Dysfunction in Circulatory Shock and Trauma.- 3.1. Failure of Local Vascular-Homeostatic Mechanisms.- 3.2. Vasoactive Mediators in Circulatory Shock and Low-Flow States.- 4. RE Cell Function in Recognition and Treatment of Circulatory Shock and Trauma.- 4.1. Overview of Circulatory Shock Problem.- 4.2. RES Phagocytic Function as a Tissue-Level Index of the Course of Shock and Low-Flow State Syndrome.- 4.3. RES-Stimulating Materials Compatible for Human Use: Prophylactic Treatment for Circulatory Shock.- 5. Specific RE Cell-Microcirculatory Interactions in Shock, Trauma, and Systemic Stress.- 5.1. RE Cell Colloid Stimulants Prevent Loss of Venular Tone in Circulatory Shock and Trauma.- 5.2. Estrogenic and Glucocorticoid Steroids Normalize Microvascular Tone in Circulatory Shock and Trauma: Temporal Relationship to Effects on the RES.- 5.3. Vasoactive Peptide Pressor Analogs with Selective Microvascular Actions Improve Survival and RE Cell Function in Shock and Trauma Syndromes.- 6. Conclusions.- References.- 16. Radiation Effects on Phagocytic Cells of the RES.- 1. Introduction.- 2. Alterations of RES Cell Structure.- 3. Changes of Phagocytic Cell Function.- 3.1. Irradiation in Vitro.- 3.2. Irradiation in Vivo.- 4. Changes of Global RES Phagocytic Function.- 4.1. Inorganic Colloids: Chromium Phosphate, Saccharated Iron Oxide, Radiogold, Thorotrast, Prodigiosin.- 4.2. Carbon Clearance.- 5. Handling of Bacteria and Antigens by Macrophages.- 5.1. Bacterial Clearance.- 5.2. Intracellular Digestive Function of Macrophages.- 6. Presentation of Antigen.- 7. Biochemical Properties.- 8. Altered Response of the RES in Whole-Body-Irradiated Animals.- 8.1. Alteration in Drug Response.- 8.2. Enhancement of Particle-Induced RES Blockade.- 8.3. Potentiation of the Response to Stress.- 8.4. Mechanisms of Depression of RES Response.- 9. Oxygen Metabolism.- 10. Protection against Radiation Lethality.- 11. Conclusion.- References.- 17. Role of the Reticuloendothelial System in Shock.- 1. Introduction.- 2. Evidence for RES Involvement in Shock.- 2.1. General Observations.- 2.2. RES Blockade.- 2.3. RES Stimulation.- 2.4. RES Activity in Shock.- 2.5. Effect of Macrophage Heterogeneity on Responses to Trauma.- 2.6. Role of the RES in Immune Suppression following Traumatic Shock.- 2.7. Effect of Trauma on RE Cells in the Lung.- 2.8. Effect of Adrenal Cortical Hormones on RES Function following Trauma.- 2.9. Effect of Other Hormones on RES Function following Trauma.- 2.10. Effect of Trauma on RE Cell Energy Metabolism.- 2.11. Effect of Starvation on Susceptibility to Shock Induction.- 2.12. Effect of Cancer on Susceptibility to Shock Induction.- 3. Effect of Trauma-Sensitive Factors on RES and Shock Induction.- 3.1. Role of Lysosomal Enzymes in the Pathogenesis of Shock.- 3.2. Effect of Released Tissue Debris on RES Function.- 3.3. Effect of Fibronectin Depletion on RES Function.- 3.4. RE Cell Depressant Substance.- 3.5. Role of Prostaglandins in Shock.- 3.6. Toxic Oxygen Products.- 4. Regulatory Role of Trauma-Sensitive Serum Factors on RES Activity.- 4.1. C-Reactive Protein.- 4.2. Ceruloplasmin.- 4.3. Role of Fibronectin in Shock.- 4.4. The Effect of Complement Activation on Shock Induction and RES Function.- 4.5. Trauma-Protecting Factors.- 4.6. Histamine.- 5. Summary: Mechanism of Shock Induction and Protective Activity of the RES.- References.- 18. Toxic Oxygen Products in Shock.- 1. Introduction.- 2. Toxic Oxygen Products.- 2.1. Cytotoxic Action.- 2.2. Inactivation of Antiproteases.- 2.3. Prostaglandin, Thromboxane, and Leukotriene Generation.- 3. Protective Mechanisms against Toxic Oxygen Products.- 3.1. Plasma Factors.- 3.2. Cellular Factors.- 4. Glutathione.- 4.1. Glutathione Deficiencies.- 4.2. Traumatic Shock.- 5. Addition of Scavengers.- 5.1. Glutathione.- 5.2. Superoxide Dismutase.- 5.3. Other Radical Scavengers.- 5.4. Corticosteroids.- 6. Complement Activation.- 7. Shock Induction.- 7.1. Anaphylatoxins.- 7.2. Toxic Oxygen Products.- 8. Summary.- References.- 19. The RES and the Turnover of Circulating Lysosomal Enzymes in Shock.- 1. Introduction.- 2. Release of Lysosomal Enzymes in Shock.- 2.1. RE Function, Shock Tolerance, and Enzyme Release.- 2.2. Role of Single Organs in Enzyme Turnover.- 2.3. Cellular Origin of Lysosomal Enzymes.- 3. RES and Enzyme Elimination.- 3.1. Lysosomal Enzymes as Shock Toxins.- 3.2. Clinical Evidence for Enzyme Elimination.- 3.3. Hepatic Receptors and Clearance of Lysosomal Enzymes.- 4. Balance of Circulating Lysosomal Enzymes.- 5. Summary.- References.