Taurine is a free amino acid rich in neutrophils, and neutrophils play an important role in the forefront defense against infection. Upon neutrophil activation, taurine reacts with hypochlorous acid (HOCl/OCl⁻) produced by the myeloperoxidase (MPO) system and gets converted to taurine chloramine (Tau-Cl). Neutrophils have three types of granules, of which the primary granule MPO, secondary granule lactoferrin, and tertiary granule matrix metalloproteinase (MMP)-9 are released into the extracellular space by a process called degranulation. MPO produces hypochlorous acid to kill microorganisms, and the released MPO forms neutrophil extracellular traps (NETs) with released chromatin. Excessive secretion of MPO causes oxidative damage to the surrounding tissues. Lactoferrin exerts antioxidant activity, prevents pro-inflammatory pathway activation, sepsis, and tissue damages, and delays neutrophil apoptosis. Our experimental results show that neutrophils released small amount of granules in an inactive state, and phorbol 12-myristate 13-acetate (PMA) and N-formyl-methionine-leucyl-phenylalanine induced neutrophil degranulation. Tau-Cl inhibited the PMA-induced degranulation of MPO and formation of NETs. While Tau-Cl increased the degranulation of lactoferrin, it had no effect on MMP-9 degranulation. MPO negatively regulated the production of macrophage inflammatory protein (MIP)-2, which stimulates the degranulation and migration of neutrophils. Tau-Cl abrogated MIP-2 expression, suggestive of its inhibitory effect on MPO release. The increase in the intracellular level of MPO may negatively regulates MIP-2 expression, thereby contributing to the further regulation of neutrophil degranulation and migration. Here, we suggest that Tau-Cl selectively inhibits MPO degranulation and stimulates lactoferrin degranulation from neutrophils, thereby protecting inflamed tissues from oxidative damage induced by excessively released MPO.

牛磺酸是富含嗜中性粒细胞的游离氨基酸，嗜中性粒细胞在最前沿的抗感染防御中起着重要作用。一旦嗜中性粒细胞活化，与次氯酸（HOCl / OCL牛磺酸起反应^-）由髓过氧化物酶（MPO）系统产生，并转化为牛磺酸氯胺（Tau-Cl）。中性粒细胞具有三种类型的颗粒，其中初级颗粒MPO，次级颗粒乳铁蛋白和第三级颗粒基质金属蛋白酶（MMP）-9通过称为脱粒的过程释放到细胞外空间。MPO产生次氯酸以杀死微生物，释放的MPO与释放的染色质形成嗜中性白细胞胞外陷阱（NETs）。MPO分泌过多会引起周围组织的氧化损伤。乳铁蛋白发挥抗氧化活性，防止促炎途径激活，败血症和组织损伤，并延迟中性粒细胞凋亡。我们的实验结果表明，中性粒细胞在非活性状态下释放出少量颗粒，而佛波醇12-肉豆蔻酸酯13-乙酸酯（PMA）和ñ-甲酰基-蛋氨酸-亮氨酸-苯丙氨酸诱导中性粒细胞脱粒。Tau-Cl抑制PMA诱导的MPO脱粒和NETs的形成。尽管Tau-Cl增加了乳铁蛋白的脱颗粒，但它对MMP-9的脱颗粒没有影响。MPO负调节巨噬细胞炎症蛋白（MIP）-2的产生，它刺激嗜中性粒细胞的脱粒和迁移。Tau-C1废除了MIP-2的表达，提示其对MPO释放的抑制作用。MPO的细胞内水平的增加可能负调控MIP-2表达，从而有助于中性粒细胞脱粒和迁移的进一步调控。在这里，我们建议Tau-Cl选择性抑制MPO脱粒并刺激嗜中性粒细胞的乳铁蛋白脱粒，