Fever and Inflammation in Nonspecific Immunity Saved

Fever

Promotes interferon activity, accelerates metabolic rate and tissue repair, inhibits pathogen reproduction.

Pyrogens

Fever-producing agents that trigger fever.

Exogenous pyrogens

Glycolipids on bacterial and viral surfaces.

Interleukins

Released by neutrophils and macrophages, they stimulate neurons in the anterior hypothalamus.

PGE2

Raises hypothalamic set point for body temperature.

Antipyretics

Substances like aspirin that reduce fever by inhibiting PGE2.

Stages of fever

Onset, Stadium, Defervescence.

Onset

Pyrogens raise the hypothalamic set point, body temperature begins to rise.

Stadium

Temperature oscillates around the high set point while infection persists.

Defervescence

Infection ends, set point returns to normal, and body temperature decreases.

Functions of inflammation

Defensive response to tissue injury, limits pathogen spread, destroys pathogens, removes debris, initiates tissue repair.

Classic signs of inflammation

Erythema, Edema, Heat, Pain.

Erythema

Redness from increased blood flow (hyperemia).

Edema

Swelling due to increased capillary permeability.

Heat

From hyperemia.

Pain

From inflammatory chemicals and pressure on nerves.

Suffix '-itis'

Indicates inflammation of a specific organ (e.g., tonsillitis, arthritis).

Suffix '-algia'

Indicates pain (e.g., neuralgia = nerve pain).

Cytokines

Chemicals that regulate inflammation and immunity, altering the physiology or behavior of the receiving cell.

Major processes of inflammation

Mobilization of body defenses, containment and destruction of pathogens, tissue cleanup and repair.

Mobilization of defenses

Immediate response to bring leukocytes to infection site, local hyperemia, local vasodilation caused by histamine, leukotrienes, and cytokines.

Hyperemia

Increased blood flow that speeds delivery of immune cells and washes toxins.

Margination

WBCs adhere to blood vessel walls.

Diapedesis

WBCs crawl between endothelial cells into tissue fluid.

Increased capillary permeability

Caused by vasoactive chemicals dilating blood vessels and endothelial cells separating, allowing fluid, leukocytes, and plasma proteins to enter tissue.

Containment and destruction phase

Goal is to prevent spread of pathogens; fibrinogen forms a sticky mesh to isolate pathogens.

Heparin

Prevents clotting in inflamed area so WBCs can move.

Neutrophils

Arrive first to kill bacteria via phagocytosis and respiratory bursts.

Monocytes

Arrive later and take over cleanup and tissue repair.