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The inflammatory response can be provoked by physical, chemical, and biologic agents, including mechanical trauma, exposure to excessive amounts of sunlight, x-rays and radioactive materials, corrosive chemicals, extremes of heat and cold, or by infectious agents such as bacteria, viruses, and other pathogenic microorganisms. Although these infectious agents can produce inflammation, infection and inflammation are not synonymous.
The classic signs of inflammation are heat, redness, swelling, pain, and loss of function. These are manifestations of the physiologic changes that occur during the inflammatory process. The three major components of this process are (1) changes in the caliber of blood vessels and the rate of blood flow through them (hemodynamic changes); (2) increased capillary permeability; and (3) leukocytic exudation.
Hemodynamic changes begin soon after injury and progress at varying rates, according to the extent of injury. They start with dilation of the arterioles and the opening of new capillaries and venular beds in the area. This causes an accelerated flow of blood, accounting for the signs of heat and redness. Next follows increased permeability of the microcirculation, which permits leakage of protein-rich fluid out of small blood vessels and into the extravascular fluid compartment, accounting for the inflammatory edema.
Leukocytic exudation occurs in the following sequence. First, the leukocytes move to the endothelial lining of the small blood vessels (margination) and line the endothelium in a tightly packed formation (pavementing). Eventually, these leukocytes move through the endothelial spaces and escape into the extravascular space (emigration). Once they are outside the blood vessels they are free to move and, by chemotaxis, are drawn to the site of injury. Accumulations of neutrophils and macrophages at the area of inflammation act to neutralize foreign particles by phagocytosis.
Chemical mediators of the inflammatory process include a variety of substances originating in the plasma and the cells of uninjured tissue, and possibly from the damaged tissue. The major kinds of mediators are (1) vasoactive amines, such as histamine and serotonin; (2) plasma endopeptidases that comprise three interrelated systems, the kinin system that produces bradykinin, the complement system that produces proteins that interact with antigen--antibody complexes and mediate immunologic injury and inflammation, and the clotting system that increases vascular permeability and chemotactic activity for the leukocytes; (3) prostaglandins, which can reproduce several aspects of the inflammatory process; (4) neutrophil products; (5) lymphocyte factors; and (6) other mediators, such as slow-reacting substance of anaphylaxis and endogenous pyrogen.
Hormonal Response. Some hormones, such as cortisol, have an antiinflammatory action that limits inflammation to a local reaction while others are proinflammatory. Thus, the endocrine system has a regulatory effect on the process of inflammation so that it can be balanced and beneficial in the body's attempts to recover from injury.
pro·lif·er·a·tive in·flam·ma·tion(prō-lif'ĕr-ă-tiv in'flă-mā'shŭn)
Synonym(s): hyperplastic inflammation.
inflammation(in?fla-ma'shon) [L. inflammare, to kindle]
The Inflammatory Process
Local inflammatory responses begin when traumatized or infected tissues activate the humoral and cellular immune systems. Complement proteins and cytokines are manufactured. These signaling proteins start a cascade of chemical events that result in increases in local blood flow and the attraction of white blood cells to the damaged tissue. White blood cells in turn consume foreign or injured cells and release arachidonic acid metabolites, kinins, histamines, and more complement, thereby amplifying and perpetuating the immune response. The white blood cells also release toxic oxygen radicals, nitric oxide, and tissue-destroying enzymes in an attempt to kill any invading microorganisms. In healthy people, the process continues until all damaged tissues or invading pathogens are removed (usually about 5 days); an inpouring of fibroblasts, which repair the injury and form a healed scar, follows.
Systemic inflammatory responses occur when foreign proteins are recognized, e.g., in the bloodstream, and immune complexes are formed or cytotoxic T cells are activated. If sepsis triggers the immune response, these agents may help clear microorganisms from the blood.
Autoimmune illnesses occur when the chemical and cellular tools of inflammation are directed against the body's own tissues.
Nonspecific test results that suggest inflammation include an elevated white blood cell count, erythrocyte sedimentation rate, or C-reactive protein level.
Mild inflammation (such as the inflammatory change from minor injuries) often resolves with the topical application of ice packs or cold water. Nonsteroidal anti-inflammatory drugs (such as ibuprofen) and steroids (such as prednisone) are useful in managing more severe inflammation, as are many disease-modifying antirheumatic drugs, such as methotrexate or azathioprine.
inflammation of jejunumJejunitis.
inflammation of liverHepatitis.
proliferative inflammationHyperplastic inflammation.
suppurative inflammationPurulent inflammation.
|Arachidonic acid metabolites (prostaglandins and leukotrienes)||Phospholipids of cell membranes, especially mast cells||Primary mediators of late-stage (> 6 hr) inflammation; increase dilation and permeability of blood vessels; stimulate neutrophil adhesion to endothelial tissue; bronchoconstriction; anaphylaxis|
|Bradykinin||Kinin system of plasma proteins||Primary mediator of prolonged (> 1 hr) inflammation; vasodilation and increased permeability of blood vessels; pain; release of leukotrienes and prostaglandins|
|Complement proteins||Macrophages; liver endothelium||Increase vasodilation and vascular permeability; coat antigens to enhance phagocytosis; attract neutrophils; destroy pathogens|
|Histamine and serotonin||Mast cells; basophils||Primary mediators of early (=30 min) inflammation; rapid dilation and increase in permeability of venules; bronchoconstriction; stimulation of prostaglandin production|
|Interleukin 1 (IL-1)||Macrophages; B cells, dendritic cells, neutrophils, other nucleated cells||Increased production and activity of other chemical mediators, phagocytes and lymphocytes; promotes release of acute-phase proteins; causes fever|
|Interleukin 8 (IL-8)||T lymphocytes; monocytes||Attracts neutrophils and more T cells|
|Platelet-activating factor (PAF)||Platelets||Releases chemical mediators; activates neutrophils; dilates and increases permeability of vessels|
|Transforming growth factor ß (TFGß)||Activated macrophages and T lymphocytes||Attracts neutrophils and monocytes; stimulates growth of connective tissue; inhibits other mediators|
|Tumor necrosis factors (TFNa)||Activated macrophages and some lymphocytes||Increase synthesis of other cytokines; induce formation of new blood vessels; increase adhesion of neutrophils to endothelium; cause fever and cachexia|