Bieth J G
Eur J Respir Dis Suppl. 1985;139:57-61.
The protease-antiprotease theory of pulmonary emphysema holds that alveolar structures may be destroyed by neutrophil elastase but are normally protected from destruction by elastase inhibitors. Bronchoalveolar lavage allows to collect three types of antielastases: alpha 1-proteinase inhibitor (alpha 1 PI), bronchial mucus inhibitor and "unidentified inhibitors". Alpha 1 PI acts as an irreversible inhibitor of serine-proteinases. It reacts much faster with neutrophil elastase than with other enzymes and is therefore considered as a physiological inhibitor of this leukoproteinase. Oxidation of Met into methionine sulfoxide leads to a dramatic reduction of the inhibitory capacity of alpha 1 PI. This oxidative inactivation may be brought about by oxidants excreted by phagocytes and cigarette smoke condensate. A back-up control is provided by methionine sulfoxide reductase, an enzyme present in phagocytes and capable of reducing oxidized alpha 1 PI. The bronchial inhibitor is an acid-stable protein secreted by the mucus cells of the respiratory tract. It is a reversible tight-binding inhibitor which reacts with neutrophil elastase. Although it occurs in low amounts in the lower respiratory tract it may play an active physiological role because of its low molecular weight which allows its easy diffusion within the interstitial tissue.
肺气肿的蛋白酶 - 抗蛋白酶理论认为，肺泡结构可能会被中性粒细胞弹性蛋白酶破坏，但通常会受到弹性蛋白酶抑制剂的保护而不被破坏。支气管肺泡灌洗可收集三种抗弹性蛋白酶：α1 - 蛋白酶抑制剂（α1 PI）、支气管黏液抑制剂和“未鉴定的抑制剂”。α1 PI作为丝氨酸蛋白酶的不可逆抑制剂。它与中性粒细胞弹性蛋白酶的反应比与其他酶的反应快得多，因此被认为是这种白细胞蛋白酶的生理抑制剂。甲硫氨酸氧化为甲硫氨酸亚砜会导致α1 PI的抑制能力急剧下降。这种氧化失活可能由吞噬细胞分泌的氧化剂和香烟烟雾冷凝物引起。甲硫氨酸亚砜还原酶提供了一种后备控制机制，这种酶存在于吞噬细胞中，能够还原被氧化的α1 PI。支气管抑制剂是一种由呼吸道黏液细胞分泌的耐酸蛋白。它是一种与中性粒细胞弹性蛋白酶反应的可逆紧密结合抑制剂。尽管它在下呼吸道中的含量较低，但由于其分子量低，易于在间质组织中扩散，可能发挥积极的生理作用。
