Chemical Mediators Of The Acute Inflammatory Reaction

International Series of Monographs in Pure and Applied Biology, Modern Trends in Physiological Sciences, Volume 37: Chemical Mediators of the Acute Inflammatory Reaction traces the history of investigation into the acute inflammatory reaction from the early observations in invertebrates to the experiments of therapeutic significance for humans. This book focuses on mediators that are accepted as being commonly involved in the inflammatory reaction, such as histamine, kinins, serotonin, prostaglandins, and permeability factors. The topics discussed include the phagocytic system and antibody production; factors which influence phagocytosis; measurement of the acute inflammatory reaction; and combined actions of mediators. The reaction to injury and manifestation of inflammation and biochemical aspects of anti-inflammatory drug reaction are also covered. This volume is beneficial to anatomists, biochemists, physiologists, immunologists, pathologists, pharmacologists, and clinicians interested in acute inflammatory reaction.

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. This book provides an introduction to the cell types, chemical mediators, and general mechanisms of the host's first response to invasion.

With contributions by numerous experts

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.

Provides an introduction to the cell types, chemical mediators, and general mechanisms of the host's first response to invasion.