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[L. inflammare, to kindle]
An immunological defense against injury, infection, or allergy, marked by increases in regional blood flow, immigration of white blood cells, and release of chemical toxins. Inflammation is one way the body uses to protect itself from invasion by foreign organisms and to repair wounds to tissue. Clinical hallmarks of inflammation are redness, heat, swelling, pain, and loss of function of a body part. Systemically, inflammation may produce fevers, joint and muscle pains, organ dysfunction, and malaise.
SYN: SEE: inflammatory response SEE TABLE: Mediating Factors in Inflammation; SEE: autoimmune disease; SEE: infection

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.

Mediating Factors in Inflammation
Arachidonic acid metabolites (prostaglandins and leukotrienes)Phospholipids of cell membranes, especially mast cellsPrimary mediators of late-stage (>6 hr) inflammation; increase dilation and permeability of blood vessels; stimulate neutrophil adhesion to endothelial tissue; bronchoconstriction; anaphylaxis
BradykininKinin system of plasma proteinsPrimary mediator of prolonged (>1 hr) inflammation; vasodilation and increased permeability of blood vessels; pain; release of leukotrienes and prostaglandins
Complement proteinsMacrophages; liver endotheliumIncrease vasodilation and vascular permeability; coat antigens to enhance phagocytosis; attract neutrophils; destroy pathogens
Histamine and serotoninMast cells; basophilsPrimary 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 cellsIncreased production and activity of other chemical mediators, phagocytes and lymphocytes; promotes release of acute-phase proteins; causes fever
Interleukin 8 (IL-8)T lymphocytes; monocytesAttracts neutrophils and more T cells
Platelet-activating factor (PAF)PlateletsReleases chemical mediators; activates neutrophils; dilates and increases permeability of vessels
Transforming growth factor β (TFGβ)Activated macrophages and T lymphocytesAttracts neutrophils and monocytes; stimulates growth of connective tissue; inhibits other mediators
Tumor necrosis factors (TFNα)Activated macrophages and some lymphocytesIncrease synthesis of other cytokines; induce formation of new blood vessels; increase adhesion of neutrophils to endothelium; cause fever and cachexia

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