Mechanism of defence

Mechanism of defence:

Inflammatory response is a collective term representing the complex sequence of events during inflammation. It initiates when injured tissue cells release inflammatory mediators
(chemicals). Among the inflammatory mediators are various serum proteins called acute-phase proteins; the principal acute-phase proteins are histamine and kinins.

The acute-phase proteins bind to receptors on nearby capillaries and venules causing vasodilation and increased permeability which results in influx of phagocytes (e.g., neutrophils, lymphocytes monocytes and macrophages) from the blood into the tissues.

The emigration of phagocytes is a multistep process (Fig. 44.14) that includes adherence of the cells to the endothelial wall of the blood vessels (margination), followed by their emigration between endothelial cells in to the tissues (diapedesis or extravasation), and finally, their migration through the tissue to the site of the invasion (chemotaxis).

As the phagocytic cells accumulate in the site of injury and begin to phagocytose microbial pathogens, during this process they release lytic enzymes that normally damage the nearby healthy cells. Dead host cells, dead phagocytic cells, dead microbial pathogens, and the body fluid collectively form a substance called pus (the inflammatory exudate).

When the acute-phase proteins bind to receptors on nearby capillaries and venules and cause vasodilation and increased permeability, the latter 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, a main constituent 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 is subsided and the pus is removed, the infected or injured area is filled with new tissues that start normal function.