INHIBITION OF NEUTROPHIL SUPEROXIDE PRODUCTION BY HUMAN PLASMA ALPHA-1-ANTITRYPSIN
INHIBITION OF NEUTROPHIL SUPEROXIDE PRODUCTION BY HUMAN PLASMA ALPHA-1-ANTITRYPSIN
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DOI：
10.1016/0014-5793(92)80156-b
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发表时间：
1992-03-23
期刊：
影响因子：
3.5
通讯作者：
WINYARD, PG
中科院分区：
文献类型：
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作者：
BUCURENCI, N;BLAKE, DR;WINYARD, PG
我们报道了人血浆α-1-抗胰蛋白酶(α-1-AT)抑制由多种兴奋剂引起的人中性粒细胞O2.释放。两种丝氨酸蛋白酶抑制剂L-1-对甲苯磺酰胺-2-苯乙基氯甲基酮(TPCK)和大豆胰酶抑制剂(SBTI)与人重组α-1-AT突变体α-1-AT-Arg358的抑制能力大小顺序为：α-1-AT几乎等于TPCK，远大于α-1-AT-Arg358>；这些数据表明，在含有相对较高浓度的α-1-AT的人类炎性液体(如类风湿性关节炎滑液)中，(I)α-1-AT可能通过抑制中性粒细胞呼吸爆发而下调炎症过程，(Ii)中性粒细胞释放的活性氧物种不太可能发生丝氨酸氧化。
We report here that human plasma alpha-1-antitrypsin (alpha-1-AT) inhibited human neutrophil O2.- release elicited by a variety of stimulants. In comparison, the inhibitory capacities of two serine protease inhibitors, L-1-tosylamide 2-phenylethyl chloromethyl ketone (TPCK) and soybean trypsin inhibitor (SBTI), and the human recombinant alpha-1-AT mutant, alpha-1-AT-Arg358 were in the order: alpha-1-AT almost-equal-to TPCK much greater than alpha-1-AT-Arg358 > SBTI when cells were stimulated with concanavalin A plus cytochalasin E. These data suggest that, in human inflammatory fluids containing relatively high concentrations of alpha-1-AT (such as rheumatoid arthritis synovial fluid), (i) alpha-1-AT may down-regulate the inflammatory process by inhibiting the neutrophil respiratory burst and (ii) serpin oxidation by neutrophil-released reactive oxygen species is unlikely to occur.