What is inflammation?
In inflammation, the following changes are seen locally: redness, swelling, heat, pain, and loss of function. These changes are chemically mediated. Inflammation may be caused by microbial infection; physical agents such as trauma, radiation, and burns; chemical toxins; caustic substances such as strong acids or bases; decomposing or necrotic tissue; and reactions of the immune system. Acute inflammation is of relatively short duration (from a few minutes to a day), while chronic inflammation lasts longer. The local changes associated with inflammation include the outflow of fluid into the spaces between cells and the inflow or migration of white blood cells (leukocytes) to the area of injury. Chronic inflammation is characterized by the presence of leukocytes and macrophages, as well as by the proliferation of new blood vessels and connective tissue.
Inflammation is a protective mechanism for the body. Redness is attributable to increased blood flow to the injured area. Swelling is caused by the flow of fluid into the spaces between cells. Heat is produced by a combination of increased blood flow and chemical reactions in the local area. Pain results from the presence of two main chemicals found in the bloodstream: prostaglandins and bradykinin. Loss of function is a result of pain (the body limits movement to reduce discomfort) and swelling (interstitial fluid limits movement).
Acute inflammation. Many chemicals are involved in acute inflammation. Mediators of inflammation originate from blood plasma and from both damaged and normal cells. Vasoactive amines are a class of chemicals that increase the permeability of blood vessel and cell walls. The most well studied of these are histamine and serotonin. Histamine is stored in granules in mast cells that are found in both tissue and basophils, the latter being a type of cell found in the blood. Serotonin is found in mast cells and platelets; it is another type of cell found in the bloodstream. These substances cause vasodilation (expansion of the walls of blood vessels) and increased vascular permeability (leakage through the walls of small vessels, especially veins). Histamine and serotonin can be released by traumaor exposure to cold. Other chemicals that circulate in the blood can release histamine. Two of these are part of the complement system; another is called interleukin-1. The effects of histamine diminish after approximately one hour.
Plasma proteases comprise three interrelated systems that explain much that is known about inflammation: the complement, kinin, and clotting systems. The complement system is composed of twenty different proteins involved in reactions against microbial agents that invade the body. The various chemicals act in a cascade, similar to falling dominoes: Each one sets off another in sequence. The result of these chemical actions is to increase vascular permeability, promote chemotaxis (the attraction of living cells to specific chemicals), engulf invading microorganisms, and destroy pathogens through a process called lysis.
The kinin system is responsible for releasing bradykinin, a chemical substance that causes contraction of smooth muscle tissue, dilation of blood vessels, and pain. The duration of action for bradykinin is brief because it is inactivated by the enzyme kininase. Bradykinin does not promote chemotaxis.
The clotting system is made up of a series of chemicals that result in the formation of a solid mass. The most commonly encountered example is the scab that forms at the site of a cut in the skin. Like the complement system, the clotting system is a cascade of thirteen different chemicals. In addition to producing a solid mass, the clotting system increases vascular permeability and promotes chemotaxis for white blood cells.
Other substances are involved in acute inflammation. Among the most important of these is a class called prostaglandins. Several different prostaglandin molecules have been isolated; they are derived from the membranes of most cells. Prostaglandins cause pain, vasodilation, and fever. Aspirin counteracts the effects of prostaglandins, which explains the antipyretic (fever-reducing) and analgesic (pain-reducing) properties of the drug.
Another group of substances involved in acute inflammation are leukotrienes. The primary sources for these molecules are leukocytes, and some leukotrienes are found in mast cells. This group promotes vascular leakage but not chemotaxis. They also cause vasoconstriction (a decrease in the diameter of blood vessels) and bronchoconstriction (a decrease in the diameter of air passageways in the lungs). The effect of these leukotrienes is to slow blood flow and restrict air intake and outflow. A different type of leukotriene is found only in leukocytes. This type enhances chemotaxis but does not contribute to vascular leakage. In addition, leukotrienes cause white blood cells to stick to damaged tissues, speeding the removal of bacteria and promoting healing.
Other chemical substances are known to be involved with inflammation: platelet-activating factor, tumor necrosis factor, interleukin-1, cationic (positively charged) proteins, neutral proteases (enzymes that break down proteins), and oxygen metabolites (molecules resulting from reactions with oxygen). The sources of these are generally leukocytes, although some are derived from macrophages. They reinforce the effects of prostaglandins and leukotrienes.
There are four different outcomes for acute inflammation. There may be complete resolution in which the injured site is restored to normal; this outcome usually follows a mild injury or limited trauma where there has been only minor tissue destruction. Healing with scarring may occur, in which injured tissue is replaced with scar tissue that is rich in collagen, giving it strength but at the cost of normal function; this outcome follows more severe injury or extensive destruction of tissue. There may be the formation of an abscess, which is characterized by pus and which follows injuries that become infected with pyogenic (pus-forming) organisms. The fourth outcome is chronic inflammation.
Chronic inflammation. Acute inflammation may be followed by chronic inflammation. This reaction occurs when the organism, factor, or agent responsible for the acute inflammation is not removed or when the normal processes of healing fail to occur. Repeated episodes of acute inflammation may also lead to chronic inflammation, in which the stages of acute inflammation seem to remain for long periods of time. In addition, chronic inflammation may begin insidiously, such as with a low-grade infection or other process that does not display the usual signs of acute inflammation; tuberculosis, rheumatoid arthritis, and chronic lung disease are examples of this third alternative.
Chronic inflammation typically occurs in one of the following conditions: prolonged exposure to potentially toxic substances such as asbestos, coal dust, and silica that are nondegradable; immune reactions against one’s own tissue (autoimmune diseases such as lupus and rheumatoid arthritis); and persistent infection by an organism that is either resistant to drug therapy or insufficiently toxic to cause an immune reaction (such as viruses, tuberculosis, and leprosy). The characteristics of chronic inflammation are similar to those of acute inflammation but are less dramatic and more protracted.
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