Kastenbauer E R, Hochstrasser K, Reichert R, Brohr T
Laryngol Rhinol Otol (Stuttg). 1977 Mar;56(3):201-6.
The proteolytic activity of different proteinases during chronic otitis media can be inhibited by alpha-2-macroglobulin and alpha-1-antitrypsin. A new low molecular (13,000) acid stable and polyvalent proteinase inhibitor could be investigated in the middle ear secretion from patients with cholesteatoma and chronic otitis media. We believe that this inhibitor is identical with the low molecular inhibitor of bronchial mucus and the nasal fluid. This inhibitor shows a high anti proteolytic capacity and can inactive trypsin, chymotrypsin, pronase and leucocytic preoteinases. The inhibitor is not detectable in any case. We could find it in 55 cases, three specimens of middle ear secretions obtained no acid stable inhibitor. It is present in the secretion in a masked form by in situ-reaction with leucocytic proteinases. By denaturating deproteinizing it is liberated out of the complex with proteinases and can be measured. The investigations demonstrate that the level of the inhibitor varies during the course of a chronic otitis media. In the postoperative phase the inhibitor concentrations were clearly higher than preoperatively. A steep drop of inhibitor can be observed in cases of chronic otitis with the symptomatology of an acute inflammation. In cases with a chronic inflammation the inhibitor level seems to remain low. The decrease of the inhibitor is explained as a using up effect during reaction between inhibitor and leucocytic proteinases. We believe that this inhibitor in the middle ear secretion results from a limited proteolysis and splitting of inter-alpha-trypsin inhibitor by a proteolytic enzyme, possibly by kallikrein.
α-2-巨球蛋白和α-1-抗胰蛋白酶可抑制慢性中耳炎期间不同蛋白酶的蛋白水解活性。一种新的低分子（13,000）酸稳定且多价的蛋白酶抑制剂可在胆脂瘤型和慢性中耳炎患者的中耳分泌物中进行研究。我们认为这种抑制剂与支气管黏液和鼻分泌物中的低分子抑制剂相同。该抑制剂具有较高的抗蛋白水解能力，可使胰蛋白酶、糜蛋白酶、链霉蛋白酶和白细胞蛋白酶失活。在任何情况下均未检测到该抑制剂。我们在55例中发现了它，3份中耳分泌物标本未获得酸稳定抑制剂。它以与白细胞蛋白酶原位反应的形式以隐蔽状态存在于分泌物中。通过变性脱蛋白，它从与蛋白酶的复合物中释放出来并可进行测量。研究表明，该抑制剂的水平在慢性中耳炎病程中有所变化。术后阶段抑制剂浓度明显高于术前。在具有急性炎症症状的慢性中耳炎病例中可观察到抑制剂急剧下降。在慢性炎症病例中，抑制剂水平似乎保持较低。抑制剂的减少被解释为抑制剂与白细胞蛋白酶反应期间的消耗效应。我们认为中耳分泌物中的这种抑制剂是由一种蛋白酶（可能是激肽释放酶）对α-胰蛋白酶抑制剂进行有限的蛋白水解和裂解产生的。
