Cortisol Prevents the Development of Inflammation by Stabilizing Lysosomes and by Other Effects Cortisol has the following effects in preventing inflammation

1. Cortisol stabilizes the lysosomal membranes. This is one of its most important anti-inflammatory effects, because it is much more difficult than normal for the membranes of the intracellular lysosomes to rupture. Therefore, most of the proteolytic enzymes that are released by damaged cells to cause inflammation, which are mainly stored in the lysosomes, are released in greatly decreased quantity.

2. Cortisol decreases the permeability of the capillaries, probably as a secondary effect of the reduced release of proteolytic enzymes. This prevents loss of plasma into the tissues.

3. Cortisol decreases both migration of white blood cells into the inflamed area and phagocytosis of the damaged cells. These effects probably result from the fact that cortisol diminishes the formation of prostaglandins and leukotrienes that otherwise would increase vasodilation, capillary permeability, and mobility of white blood cells.

4. Cortisol suppresses the immune system, causing lymphocyte reproduction to decrease markedly. The T lymphocytes are especially suppressed. In turn, reduced amounts of T cells and antibodies in the inflamed area lessen the tissue reactions that would otherwise promote the inflammation process.

5. Cortisol attenuates fever mainly because it reduces the release of interleukin-1 from the white blood cells, which is one of the principal excitants to the hypothalamic temperature control system. The decreased temperature in turn reduces the degree of vasodilation.

Thus, cortisol has an almost global effect in reducing all aspects of the inflammatory process. How much of this results from the simple effect of cortisol in stabilizing lysosomal and cell membranes versus its effect to reduce the formation of prostaglandins and leukotrienes from arachidonic acid in damaged cell membranes and other effects of cortisol is unclear.

Cortisol Causes Resolution of Inflammation. Even after inflammation has become well established, the administration of cortisol can often reduce inflammation within hours to a few days. The immediate effect is to block most of the factors that are promoting the inflammation. But in addition, the rate of healing is enhanced. This probably results from the same, mainly undefined, factors that allow the body to resist many other types of physical stress when large quantities of cortisol are secreted. Perhaps this results from the mobilization of amino acids and use of these to repair the damaged tissues; perhaps it results from the increased glucogenesis that makes extra glucose available in critical metabolic systems; perhaps it results from increased amounts of fatty acids available for cellular energy; or perhaps it depends on some effect of cortisol for inactivating or removing inflammatory products.

Regardless of the precise mechanisms by which the anti-inflammatory effect occurs, this effect of cortisol plays a major role in combating certain types of diseases, such as rheumatoid arthritis, rheumatic fever, and acute glomerulonephritis. All these diseases are characterized by severe local inflammation, and the harmful effects on the body are caused mainly by the inflammation itself and not by other aspects of the disease.

When cortisol or other glucocorticoids are administered to patients with these diseases, almost invariably the inflammation begins to subside within 24 hours.

And even though the cortisol does not correct the basic disease condition, merely preventing the damaging effects of the inflammatory response, this alone can often be a lifesaving measure.

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