The respiratory burst of granulocytes: modulation by inflammatory mediators and its mechanism.

Prior exposure of granulocytes to inflammatory mediators such as chemotactic factors, colony-stimulating factors and tumor necrosis factor primes the cells for enhanced activity of the respiratory burst, which appears not only to play an essential role in the increased host-defenses against invading microorganisms but also to be responsible for tissue damage at the inflammatory sites. The molecular basis for this priming is presently under investigation. Changes in one or more of the signal transduction events may lead to more efficient stimulation of the NADPH oxidase responsible for the respiratory burst. The mechanisms of priming appear to be different according to the priming stimuli: the chemotactic peptide and the Ca2+ ionophore may prime the cells by causing an increase in cytoplasmic free Ca2+; phorbol esters by activating protein kinase C; and colony-stimulating factors and tumor necrosis factor by activating the distinct mechanism, which is independent of an increase in cytoplasmic free Ca2+ and activation of protein kinase C.