Schultz W W, Bang F B
Am J Pathol. 1977 Jun;87(3):667-84.
The mechanism of laryngotracheitis virus-induced dissolution of chick nasal turbinate cartilage was studied by lysosomal enzyme histochemistry. Five-day-old chicks were infected by intranasal instillation, and changes in lysosomal enzyme distribution were followed at daily intervals through the tissue regeneration stage, Day 28. In the mucosa the lysosomes were activated beginning on Day 1, and glycerol acid phosphatase and a diffuse form of beta-glucuronidase were released concomitant with tissue cell destruction. In the chondrocytes (where glycerol acid phosphatase was absent), beginning on Day 2, particulate (lysosomal) beta-glucuronidase decreased as diffuse beta-glucuronidase increased and extended out into the matrix. The cartilage lost its metachromatic staining properties and became soft and pliable. Regeneration of the mucosa started on Day 6 and gradual reappearance of metachromatic staining of the cartilage began on Day 8 with considerable recovery of original turbinate structure by Day 12. A lysosomal membrane labilizer, vitamin A, exacerbated the cartilage pathology, whereas a stabilizer, cortisone, retarded it.
通过溶酶体酶组织化学研究了喉气管炎病毒诱导雏鸡鼻甲骨软骨溶解的机制。对5日龄雏鸡进行滴鼻感染,并在直至第28天的组织再生阶段每天跟踪溶酶体酶分布的变化。在黏膜中,溶酶体从第1天开始被激活,甘油酸磷酸酶和弥散形式的β-葡萄糖醛酸酶随着组织细胞破坏而释放。在软骨细胞中(不存在甘油酸磷酸酶),从第2天开始,颗粒状(溶酶体)β-葡萄糖醛酸酶减少,而弥散性β-葡萄糖醛酸酶增加并扩散到基质中。软骨失去其异染性染色特性,变得柔软且易弯曲。黏膜再生从第6天开始,软骨的异染性染色在第8天逐渐重新出现,到第12天鼻甲结构基本恢复。溶酶体膜不稳定剂维生素A加剧了软骨病变,而稳定剂可的松则减缓了病变。