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首页> 外文期刊>Infection and immunity >Role of tryptophan degradation in respiratory burst-independent antimicrobial activity of gamma interferon-stimulated human macrophages.
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Role of tryptophan degradation in respiratory burst-independent antimicrobial activity of gamma interferon-stimulated human macrophages.

机译：色氨酸降解在γ干扰素刺激的人类巨噬细胞的呼吸爆发非依赖性抗菌活性中的作用。

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To determine whether extracellular tryptophan degradation represents an oxygen-independent antimicrobial mechanism, we examined the effect of exogenous tryptophan on the intracellular antimicrobial activity of gamma interferon (IFN-gamma)-stimulated human macrophages. IFN-gamma readily induced normal monocyte-derived macrophages (MDM) to express indoleamine 2,3-dioxygenase (IDO) activity and stimulated MDM, alveolar macrophages, and oxidatively deficient chronic granulomatous disease MDM to degrade tryptophan. All IFN-gamma-activated, tryptophan-degrading macrophages killed or inhibited Toxoplasma gondii, Chlamydia psittaci, and Leishmania donovani. Although exogenous tryptophan partially reversed this activity, the increases in intracellular replication were variable for normal MDM (T. gondii [5-fold], C. psittaci [3-fold], L. donovani [2-fold]), chronic granulomatous disease MDM (T. gondii [2.5-fold], C. psittaci [5-fold]), and alveolar macrophages (T. gondii [1.5-fold], C. psittaci [1.5-fold]). In addition, IFN-alpha and IFN-beta also stimulated normal MDM to express IDO and degrade tryptophan but failed to induce antimicrobial activity, and IFN-gamma-treated mouse macrophages showed neither IDO activity nor tryptophan degradation but killed T. gondii and L. donovani. These results suggest that while tryptophan depletion contributes to the oxygen-independent antimicrobial effects of the activated human macrophage, in certain cytokine-stimulated cells, tryptophan degradation may be neither sufficient nor required for antimicrobial activity.
机译：为了确定细胞外色氨酸降解是否代表一种非氧依赖性抗菌机制，我们检查了外源色氨酸对γ-干扰素（IFN-γ）刺激的人类巨噬细胞的细胞内抗菌活性的影响。 IFN-γ容易诱导正常单核细胞衍生的巨噬细胞（MDM）表达吲哚胺2,3-二加氧酶（IDO）活性，并刺激MDM，肺泡巨噬细胞和氧化性慢性肉芽肿性疾病MDM降解色氨酸。所有IFN-γ激活的色氨酸降解巨噬细胞均杀死或抑制了弓形虫，鹦鹉热衣原体和利什曼原虫。尽管外源色氨酸部分逆转了这种活性，但是对于正常的MDM（弓形虫（T. gondii）[5倍]，鹦鹉热衣原体（C. psittaci）[3倍]，多诺氏乳杆菌（L. donovani）[2倍]），慢性肉芽肿病，细胞内复制的增加是可变的。 MDM（弓形虫[2.5倍]，鹦鹉热衣原体[5倍]）和肺泡巨噬细胞（弓形虫[1.5倍]，鹦鹉热衣原体[1.5倍]）。此外，IFN-α和IFN-β也刺激正常的MDM表达IDO并降解色氨酸，但未能诱导抗菌活性，并且IFN-γ处理的小鼠巨噬细胞既没有显示IDO活性也没有色氨酸降解，但杀死了弓形虫和L.。多诺瓦尼。这些结果表明，虽然色氨酸耗竭有助于活化的人类巨噬细胞的非氧依赖性抗菌作用，但在某些细胞因子刺激的细胞中，色氨酸降解可能既不充分也不要求抗微生物活性。

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