Neutrophils are involved in the tissue damage that occurs during the innate inflammatory phase of inflammatory disease. In response to injury, neutrophils migrate out of the circulating bloodstream, extravasate between endothelial cells, and move to the site of inflammation. Glucocorticoids affect the activation of neutrophils and also the functions of neutrophils, such as chemotaxis, adhesion, transmigration, apoptosis, and phagocytosis (123, 124). Glucocorticoid regulation of these functions in neutrophils is due to numerous components including regulation of cytokines.

However, lipocortin 1 also plays a pivotal role in glucocorticoid-induced responses. Glucocorticoids have a dual effect on neutrophils. On one hand, pharmacological doses are inhibitory and suppress the inflammatory response caused by neutrophil activation and migration. On the other hand, neutrophils are required for the response to bacterial infections, and as such their circulating numbers are increased by pharmacological doses of glucocorticoids through inhibition of apoptosis

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