| Research Abstract |
Blebs exhibit abnormal accumulation of elastic fibers in the organized alveoli at the bottom and usuatly, discontinuous elastic fibers in their walls. These elastic fibers reacted with anti-alpha1-antitrypsin antibody, hut elasticfibers in the normal areas surrounding blebs did not react with anti-alpha1-antitrypsin antibody. Abnormal elastic fibers with alpha1-antitrypsin did not react with anti-MMP-I, MMP-2, MMP-9, or TIMP-2 antibodies. Therefore, it is suggested that the elastic fibers ofblebs were degraded due to an imbalance between elastase and alpha1-antitrypsin, as reported previously. Fibroblasts in fibroblastic foci in the walls ofbtebs, fibroblasts in the organized alveoli at the bottom ofblebs, macrophages, bronchiolar epitheliat cells and alveolarepithelial cells all reacted with anti-MMP-1 MMP-2, MMP-9 and TIMP-2 antibodies. As compared to the fibroblasts in the organized alveoli at the bottom of blebs, the fibroblasts in the walls of blebs were big and exhibited marked reactivity for the anti-TIMP-2 antibody. These hypertrophic fibroblasts were probably myofibroblasts, because they reacted with anti-alpha-smooth muscle actin antibody. More significant deposition of type I and Ill collagen and cellular fibronectin were observed in the walls of blebs than in the organized alveoti at the bottom of blebs. Therefore, TIMP-2 is thought to play a role in extracellular matrix deposition in coordination with MMPs. Although a large amount of fibrosis is observed in the walls ofblebs, the air spaces of blebs are thought to be expandable because of the presence of degraded elastic fibers in their walls.
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