Inflammation Represents a Complex Sequence of Events That Stimulates Immune Responses

Tissue damage caused by a wound or by an invading pathogenic microorganism induces a complex sequence of events collectively known as the inflammatory response. As described above, a molecular component of a microbe, such as LPS, may trigger an inflammatory response via interaction with cell surface receptors. The end result of inflammation may be the marshalling of a specific immune response to the invasion or clearance of the invader by components of the innate immune system. Many of the classic features of the inflammatory response were described as early as 1600 bc, in Egyptian papyrus writings. In the first century ad, the Roman physician Celsus described the "four cardinal signs of inflammation" as rubor (redness), tumor (swelling), calor (heat), and dolor (pain). In the second century ad, another physician, Galen, added a fifth sign: functio laesa (loss of function). The cardinal signs of inflammation reflect the three major events of an inflammatory response (Figure 1-4):

1. Vasodilation—an increase in the diameter of blood vessels—of nearby capillaries occurs as the vessels that carry blood away from the affected area constrict, resulting in engorgement of the capillary network. The engorged capillaries are responsible for tissue redness (erythema) and an increase in tissue temperature.

Vasoactive Hormones Blood Pressure

FIGURE 1-4

Major events in the inflammatory response. A bacterial infection causes tissue damage with release of various vasoactive and chemotactic factors. These factors induce increased blood flow to the area, increased capillary permeability, and an influx of white blood cells, including phagocytes and lymphocytes, from the blood into the tissues. The serum proteins contained in the exudate have antibacterial properties, and the phagocytes begin to engulf the bacteria, as illustrated in Figure 1-3.

FIGURE 1-4

Major events in the inflammatory response. A bacterial infection causes tissue damage with release of various vasoactive and chemotactic factors. These factors induce increased blood flow to the area, increased capillary permeability, and an influx of white blood cells, including phagocytes and lymphocytes, from the blood into the tissues. The serum proteins contained in the exudate have antibacterial properties, and the phagocytes begin to engulf the bacteria, as illustrated in Figure 1-3.

2. An increase in capillary permeability facilitates an influx of fluid and cells from the engorged capillaries into the tissue. The fluid that accumulates (exudate) has a much higher protein content than fluid normally released from the vasculature. Accumulation of exudate contributes to tissue swelling (edema).

3. Influx of phagocytes from the capillaries into the tissues is facilitated by the increased permeability of the capillaries. The emigration of phagocytes is a multistep process that includes adherence of the cells to the endothelial wall of the blood vessels (margination), followed by their emigration between the capillary-endothelial cells into the tissue (diapedesis or extravasation), and, finally, their migration through the tissue to the site of the invasion (chemotaxis). As phagocytic cells accumulate at the site and begin to phagocytose bacteria, they release lytic enzymes, which can damage nearby healthy cells. The accumulation of dead cells, digested material, and fluid forms a substance called pus.

The events in the inflammatory response are initiated by a complex series of events involving a variety of chemical mediators whose interactions are only partly understood. Some of these mediators are derived from invading microorgan isms, some are released from damaged cells in response to tissue injury, some are generated by several plasma enzyme systems, and some are products of various white blood cells participating in the inflammatory response.

Among the chemical mediators released in response to tissue damage are various serum proteins called acute-phase proteins. The concentrations of these proteins increase dramatically in tissue-damaging infections. C-reactive protein is a major acute-phase protein produced by the liver in response to tissue damage. Its name derives from its pattern-recognition activity: C-reactive protein binds to the C-polysaccharide cell-wall component found on a variety of bacteria and fungi. This binding activates the complement system, resulting in increased clearance of the pathogen either by complement-mediated lysis or by a complement-mediated increase in phagocytosis.

One of the principal mediators of the inflammatory response is histamine, a chemical released by a variety of cells in response to tissue injury. Histamine binds to receptors on nearby capillaries and venules, causing vasodilation and increased permeability. Another important group of inflammatory mediators, small peptides called kinins, are normally present in blood plasma in an inactive form. Tissue injury activates these peptides, which then cause vasodilation and in creased permeability of capillaries. A particular kinin, called bradykinin, also stimulates pain receptors in the skin. This effect probably serves a protective role, because pain normally causes an individual to protect the injured area.

Vasodilation and the increase in capillary permeability in an injured tissue also enable enzymes of the blood-clotting system to enter the tissue. These enzymes activate an enzyme cascade that results in the deposition of insoluble strands of fibrin, which is the main component of a blood clot. The fibrin strands wall off the injured area from the rest of the body and serve to prevent the spread of infection.

Once the inflammatory response has subsided and most of the debris has been cleared away by phagocytic cells, tissue repair and regeneration of new tissue begins. Capillaries grow into the fibrin of a blood clot. New connective tissue cells, called fibroblasts, replace the fibrin as the clot dissolves. As fibroblasts and capillaries accumulate, scar tissue forms. The inflammatory response is described in more detail in Chapter 15.

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Responses

  • Rita
    Why does fluid form in response to inflammation?
    8 years ago
  • welde
    What is engorgement of the capillary network?
    8 years ago
  • Semhar
    What causes constricted blood flow in the fifth metatarsal?
    8 years ago
  • DINA
    What are the different inflammatory complex sequence of events that stimulates immune syatem?
    2 years ago

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