Baumgarten C R, Togias A G, Naclerio R M, Lichtenstein L M, Norman P S, Proud D
J Clin Invest. 1985 Jul;76(1):191-7. doi: 10.1172/JCI111945.
We have recently demonstrated that kinins are generated in vivo after nasal challenge with antigen of allergic, but not nonallergic, individuals. The present study was undertaken as a first step in determining the mechanism(s) of kinin formation during the allergic reaction and was directed towards establishing the availability and origin of kininogens in nasal secretions. Allergic individuals (n = 6) and nonallergic controls (n = 5) were challenged with antigen; and by using specific radioimmunoassays, nasal washes, obtained before and after challenge, were assayed for high molecular weight kininogen (HMWK), total kininogen (TK), albumin, and kinins. Dramatic increases in HMWK (1,730 +/- 510 ng/ml), TK (3,810 +/- 1035 ng/ml), kinin (9.46 +/- 1.75 ng/ml), and albumin (0.85 +/- 0.2 mg/ml) were observed after challenge of allergic individuals which correlated (P less than 0.001) with increases in histamine and N-alpha-tosyl-L-arginine methyl esterase activity and with the onset of clinical symptoms. For nonallergic individuals, levels of kininogens, albumin, and all mediators after antigen challenge were not different from base line. Linear regression analysis revealed excellent correlations (P less than 0.001 in each case) between increases in HMWK, TK, kinin, and albumin during antigen titration experiments and between the time courses of appearance and disappearance of HMWK, TK, kinin, and albumin after antigen challenge. Gel filtration revealed no evidence of degradation products of kininogens in nasal washes. For each allergic individual the ratio of HMWK/TK in postchallenge nasal washes was similar to the ratio of these two proteins in the same individual's plasma. These data suggest that, during the allergic reaction, there is an increase in vascular permeability and a transudation of kininogens from plasma into nasal secretions, where they can provide substrate for kinin-forming enzymes.
我们最近证实，变应性（而非非变应性）个体经抗原鼻腔激发后体内会生成激肽。本研究作为确定变应性反应期间激肽形成机制的第一步开展，旨在确定鼻分泌物中激肽原的可用性和来源。变应性个体（n = 6）和非变应性对照（n = 5）接受抗原激发；通过使用特异性放射免疫测定法，对激发前后获得的鼻洗液进行高分子量激肽原（HMWK）、总激肽原（TK）、白蛋白和激肽的检测。变应性个体激发后观察到HMWK（1,730±510 ng/ml）、TK（3,810±1035 ng/ml）、激肽（9.46±1.75 ng/ml）和白蛋白（0.85±0.2 mg/ml）显著增加，这些增加与组胺和N-α-对甲苯磺酰-L-精氨酸甲酯酶活性的增加以及临床症状的出现相关（P<0.001）。对于非变应性个体，抗原激发后激肽原、白蛋白和所有介质的水平与基线无差异。线性回归分析显示，在抗原滴定实验期间HMWK、TK、激肽和白蛋白的增加之间以及抗原激发后HMWK、TK、激肽和白蛋白出现和消失的时间进程之间存在极好的相关性（每种情况P<0.001）。凝胶过滤显示鼻洗液中没有激肽原降解产物的证据。对于每个变应性个体，激发后鼻洗液中HMWK/TK的比值与同一血浆中这两种蛋白质的比值相似。这些数据表明，在变应性反应期间，血管通透性增加，激肽原从血浆渗出到鼻分泌物中，在那里它们可为激肽形成酶提供底物。
