Role of tryptophan degradation in respiratory burst-independent antimicrobial activity of gamma interferon-stimulated human macrophages.

摘要: To determine whether extracellular tryptophan degradation represents an oxygen-independent antimicrobial mechanism, we examined the effect of exogenous on intracellular activity gamma interferon (IFN-gamma)-stimulated human macrophages. IFN-gamma readily induced normal monocyte-derived macrophages (MDM) to express indoleamine 2,3-dioxygenase (IDO) and stimulated MDM, alveolar macrophages, oxidatively deficient chronic granulomatous disease MDM degrade tryptophan. All IFN-gamma-activated, tryptophan-degrading killed or inhibited Toxoplasma gondii, Chlamydia psittaci, Leishmania donovani. Although partially reversed this activity, increases in replication were variable for (T. gondii [5-fold], C. psittaci [3-fold], L. donovani [2-fold]), [2.5-fold], [5-fold]), [1.5-fold], [1.5-fold]). In addition, IFN-alpha IFN-beta also IDO but failed induce IFN-gamma-treated mouse showed neither nor T. These results suggest that while depletion contributes effects activated macrophage, certain cytokine-stimulated cells, may be sufficient required activity.