The swollen area stimulates free nerve endings, causing the sensation of pain. Migration of phagocytes, namely neutrophils and monocytes, also occurs during the inflammatory reaction. Neutrophils and monocytes are amoeboid and can change shape to squeeze through capillary walls and enter tissue fluid. After monocytes appear on the scene, they differentiate into macrophages, large phagocytic cells that are able to devour as many as a hundred pathogens and still survive. Some tissues, particularly connective tissue, have resident macrophages, which routinely act as scavengers, devouring old blood cells, bits of dead tissue, and other debris. Macrophages also release colony-stimulating factors, which pass by way of blood to the red bone marrow, where the factors stimulate the production and the release of white blood cells, primarily neutrophils. Endocytic vesicles form when neutrophils and macrophages engulf pathogens. When the vesicle combines with a lysosome, a cellular organelle, the pathogen is destroyed by hydrolytic enzymes. As the infection is being overcome, some phagocytes die. These-along with dead tissue cells, dead bacteria, and living white blood cells- form pus, a whitish material. The presence of pus indicates that the body is trying to overcome an infection. Sometimes an inflammation persists, and the result is chronic inflammation that is often treated by administering anti-inflammatory agents such as aspirin, ibuprofen, or cortisone. These medications act against the chemical mediators released by the white blood cells in the damaged area. The inflammatory reaction can be accompanied by other responses to the injury. A blood clot can form to seal a break in a blood vessel. The antigens along with the released chemical mediators can move through the tissue fluid and lymph to the lymph nodes. Now lymphocytes mount a specific defense to the infection.
Natural Killer Cells
Natural killer (NK) cells kill virus-infected cells and tumor cells by cell-to-cell contact. They are large, granular lymphocytes with no specificity and no memory. Their number is not increased by prior exposure to any kind of cell.
The complement system, often simply called complement, is composed of a number of blood plasma proteins designated by the letter C and a subscript. A limited amount of activated complement protein is needed because a cascade effect occurs: Each activated protein in a series is capable of activating many other proteins. The complement proteins are activated when pathogens enter the body. The proteins “complement” certain immune responses, which accounts for their name. For example, they are involved in and amplify the inflammatory response because complement proteins attract phagocytes to the scene. Some complement proteins bind to the surface of pathogens already coated with antibodies, which ensures that the pathogens will be phagocytized by a neutrophil or macrophage. Certain other complement proteins join to form a membrane attack complex that produces holes in the walls and plasma membranes of bacteria. Fluids and salts then enter the bacterial cell to the point that it bursts. Interferon is a protein produced by virus-infected cells. Interferon binds to receptors of noninfected cells, causing them to prepare for possible attack by producing substances that interfere with viral replication. Interferon is specific to the species; therefore, only human interferon can be used in humans.
Nonspecific and Specific Defenses
Immunity includes nonspecific defenses and specific defenses. The four types of nonspecific defenses-barriers to entry, the inflammatory reaction, natural killer cells, and protective proteins-are effective against many types of infectious agents. Specific defenses are effective against a particular infectious agent.
Barriers to Entry
The skin and mucous membranes lining the respiratory, digestive, and urinary tracts serve as mechanical barriers to entry by pathogens. The secretions of oil glands contain chemicals that weaken or kill certain bacteria on the skin. The ciliated cells that line the upper respiratory tract sweep mucus and trapped particles up into the throat, where they can be swallowed or expectorated (coughed out). The acid pH of the stomach inhibits the growth of or kills many types of bacteria. The microbes that normally reside in the intestine and other areas, such as the vagina, prevent pathogens from taking up residence.
Whenever tissue is damaged by physical or chemical agents or by pathogens, a series of events occurs that is known as the inflammatory reaction. Figure 13.4 illustrates the participants in the inflammatory reaction. Mast cells, which occur in tissues, resemble basophils, one of the types of white cells found in the blood.
The inflamed area has four outward signs: redness, heat, swelling, and pain. All of these signs are due to capillary changes in the damaged area. Chemical mediators, such as histamine, released by damaged tissue cells and mast cells, cause the capillaries to dilate and become more permeable. Excess blood flow due to enlarged capillaries causes the skin to redden and become warm. Increased permeability of capillaries allows proteins and fluids to escape into the tissues, resulting in swelling.
Figure 13.4 Inflammatory reaction. Mast cells, which are related to basophils, a type of white blood cell, are involved in the inflammatory reaction. When a blood vessel is injured, mast cells release substances such as histamine. Histamine dilates blood vessels and increases their permeability so that tissue fluid leaks from the vessel. Swelling in the area stimulates pain receptors (free nerve endings). Neutrophils and monocytes (which become macrophages) squeeze through the capillary wall. These white blood cells begin to phagocytize pathogens (e.g., disease-causing viruses and bacteria), especially those combined with antibodies. Blood clotting seals off the capillary, preventing blood loss.