Potency of antileukoprotease and alpha 1-antitrypsin to inhibit degradation of fibrinogen by adherent polymorphonuclear leukocytes from normal subjects and patients with chronic granulomatous disease.
Potency of antileukoprotease and alpha 1-antitrypsin to inhibit degradation of fibrinogen by adherent polymorphonuclear leukocytes from normal subjects and patients with chronic granulomatous disease.
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抗白细胞蛋白酶和 α1-抗胰蛋白酶抑制来自正常受试者和慢性肉芽肿病患者的粘附多形核白细胞降解纤维蛋白原的效力。
DOI：
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发表时间：
1992
影响因子：
6.4
通讯作者：
W. Hanlon
中科院分区：
文献类型：
--
作者：
J. Stolk;P. Davies;J. Kramps;J. Dijkman;J. Humes;W. Knight;B. Green;R. Mumford;R. Bonney;W. Hanlon
我们研究了抗白蛋白蛋白酶（ALP）和α 1-抗胰蛋白酶（α 1AT）抑制附着在纤维蛋白原基质上的多形核白细胞（PMN）降解底物的相对功效。PMN弹性酶的活性是通过放免法测定纤维蛋白原a α链的氨基端a α(1-21)的特异性21残基裂解产物。重组肿瘤坏死因子- α (1 nM)孵育有助于PMN （1.0 × 10(6)）粘附在纤维蛋白原基质上。随后，细胞在细胞松弛素B和甲酰基蛋氨酸-亮基苯丙氨酸刺激前暴露于抑制剂中。在这些条件下，ALP抑制α(1-21)形成的IC50为85 +/- 30 nM， α 1AT抑制α(1-21)形成的IC50为220 +/- 98 nM（平均+/- SD）。通过比较正常受试者和x -联NADPH氧化酶缺乏症受试者的PMN对A - α(1-21)形成的影响来评估氧化剂产生对A - α(1-21)形成的影响。以上述类似的方式刺激后一种受试者的PMN，导致形成40 +/- 4 pmol/ml a α(1-21)，大约是正常受试者细胞的两倍。与ALP或α 1AT在10至900 nM浓度范围内预孵育，ALP的IC50为50 +/- 13 nM， α 1AT的IC50为150 +/- 21 nM。这两种抑制剂在预防慢性肉芽肿病（CGD） PMN引起的纤维蛋白原降解方面比正常PMN更有效，尽管CGD PMN比正常PMN产生更多的α(1-21)。（摘要删节250字）
We have studied the relative efficacy of antileukoprotease (ALP) and alpha 1-antitrypsin (alpha 1AT) to inhibit the degradation of substrate by polymorphonuclear leukocytes (PMN) attached onto a fibrinogen matrix. PMN elastase activity was assayed by radioimmunoassay of a specific 21-residue cleavage product from the amino terminus of the A alpha chain, A alpha (1-21), of fibrinogen. The adherence of PMN (1.0 x 10(6)) to a fibrinogen matrix was facilitated by incubation with recombinant tumor necrosis factor-alpha (1 nM). Subsequently, the cells were exposed to inhibitors before stimulation with cytochalasin B and formylmethionyl-leucylphenylalanine. Under these conditions, ALP inhibited A alpha (1-21) formation with an IC50 of 85 +/- 30 nM and alpha 1AT gave an IC50 of 220 +/- 98 nM (mean +/- SD). The effect of oxidant production on A alpha (1-21) formation was evaluated by comparing the effect of PMN from normal subjects with PMN from subjects with X-linked NADPH oxidase deficiency. Stimulation of PMN from the latter subjects in a similar fashion as described above resulted in the formation of 40 +/- 4 pmol/ml A alpha (1-21), or approximately twice the amount seen with cells from normal subjects. Preincubation with ALP or alpha 1AT in a concentration range between 10 to 900 nM resulted in an IC50 of 50 +/- 13 nM for ALP compared with 150 +/- 21 nM for alpha 1AT. Both inhibitors are more effective to prevent fibrinogen degradation caused by chronic granulomatous disease (CGD) PMN than by normal PMN despite the fact that CGD PMN generated more A alpha (1-21) than did normal PMN.(ABSTRACT TRUNCATED AT 250 WORDS)
抑制与弹性蛋白结合的人白细胞弹性蛋白酶：相对无效和两种抑制活性机制。
DOI：
10.1165/ajrcmb/2.3.263
发表时间：
1990
影响因子：
6.4
作者：
Morrison,HM;Welgus,HG;Stockley,RA;Burnett,D;Campbell,EJ
通讯作者：
Campbell,EJ
影响因子：
15.9
作者：
NATHAN, CF
通讯作者：
NATHAN, CF