Inflammatory Barriers

Inflammatory Barriers

Tissue damage caused by a wound or by an invading pathogenic microorganism induces a complex sequence of events collectively called as the inflammatory response. As early as the first century AD, the Roman physician Celsus described the “five cardinal signs of infection” as rubor (redness), tumor (swelling), calor (heat), dolor (pain) and functio laesa (loss of function). The cardinal signs of inflammation reflect the major events of an inflammatory response.

1.           Vasodilation: An increase in the diameter of blood vessels of nearby capillaries occurs. The vessels that carry blood away from the af-fected area constrict. This results in engorgement of the capillary network. The engorged capillaries are responsible for tissue red-ness (erythema) and in increase in tissue temperature.

2.           An increase in capillary permeability facilitates an influx of fluid and cells from the engorged capillaries into the tissue. The fluid that accumulates (exudates) has a much higher protein content. Accu-mulation of fluid contributes to tissue swelling (edema).

3.           Influx of phagocytes from the capillaries into the tissue is facilitated by the increased capillary permeability. As phagocytic cells accu-mulate at the site and begin to phagocytose bacteria, they releaselytic enzymes, which can damage nearby healthy cells. The accu-mulation of dead cells, digested material, and fluid forms a sub-stance called pus.

       The events in the inflammatory response are initiated by a com-plex series of events. During the inflammatory response, many chemi-cal mediators are released, in response to tissue damage. They are 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. Another media-tor of the inflammatory response is histamine, a chemical released by a variety of cells in response to tissue damage. Histamine causes va-sodilation and increased permeability. Another important group of in- flammatory mediators are called They are normally present in blood plasma in an inactive form. Tissue injury activates these pep-tides, which then cause vasodilation and increased permeability. A par-ticular kinin, called bradykinin, also stimulates pain receptors in the skin. Vasodilation and the increase in capillary permeability in an in-jured 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.. 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 and capillar-ies accumulate, and scar tissue forms.