Understanding Local Inflammation and Fever Response

Local Inflammation

1. Occurs when bacteria enter a break in the skin.
2. Inflammatory reaction is initiated by nonspecific mechanisms of phagocytosis and complement activation.
3. Complement activation attracts phagocytes to the area.
4. As inflammation progresses, B cells produce antibodies against bacterial antigens.
5. Attachment of antibodies to antigens amplifies nonspecific responses because of complement activation.
6. Promotes phagocytic activity of neutrophils, macrophages, and monocytes (through opsonization).
7. In the inflamed area, leukocytes attach to the surface of endothelial cells.
8. Move by chemotaxis to the inflamed site.

• Neutrophils arrive first, then monocytes, then T cells.
  • Undergo extravasation (the entire process of movement of leukocytes from the bloodstream to tissue).
• Mast cells secrete heparin, histamine, prostaglandins, leukotrienes, cytokines, and TNF-a.
  • These produce redness, warmth, swelling, pus, and pain.
  • Recruit more leukocytes.
• If the infection continues, endogenous pyrogens are released.
  • Vasodilation and increased permeability of blood vessels.
    • Results in more fluid in tissue (edema).
  • The release of histamine, kinins, and prostaglandins causes vasodilation and increased permeability of blood vessels.
• Blood clots can form around an abscess to prevent dissemination of the infection.
• Pus is the accumulation of damaged tissue and dead microbes, granulocytes, and macrophages.

Phagocyte Migration and Phagocytosis

1. Phagocytes have the ability to stick to the lining of the blood vessels (margination).
2. They also have the ability to squeeze through blood vessels (diapedesis).

Fever

Fever is an abnormally high body temperature produced in response to a bacterial or viral infection.

1. A chill indicates a rising body temperature; crisis (sweating) indicates that the body's temperature is falling.
2. Appears to be a component of innate immunity.
3. Occurs when the hypothalamic thermostat is reset upwards by interleukin-1β and other cytokines (endogenous pyrogens).

Pyrogens are released by WBCs in response to endotoxin from gram-negative bacteria (exogenous pyrogens).

1. Cytokines also increase sleepiness and a fall in the plasma Fe concentration, which functions in inhibiting bacterial activity.