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由粘质沙雷氏菌性角膜炎和一种沙雷氏菌蛋白酶引起的兔角膜损伤的特征

Characterization of rabbit corneal damage produced by Serratia keratitis and by a serratia protease.

作者信息

Lyerly D, Gray L, Kreger A

出版信息

Infect Immun. 1981 Sep;33(3):927-32. doi: 10.1128/iai.33.3.927-932.1981.

Abstract

The structural alterations elicited in the rabbit corneal stroma by experimental Serratia marcescens keratitis and by a highly purified serratia protease preparation were compared by gross observation, biochemical analyses, and electron microscopic examination of the affected tissue. Acute inflammation, liquefactive necrosis of the cornea, and descemetocele formation occurred during the development of the infection and after the intracorneal injection of submicrogram amounts of the protease. In vitro incubation of insoluble corneal stromal tissue with the bacterium or with the protease resulted in solubilization of the stromal proteoglycan ground substance; however, specific collagenase activity was not detected. Electron microscopic examination of corneas damaged by the bacterial infection and by the protease revealed loss of ruthenium red staining of the proteoglycan ground substance and dispersal of ultrastructurally normal collagen fibrils. Thus, our findings indicate that the major corneal damage which occurs during serratia keratitis and after the injection of the serratia protease is caused by solubilization and loss of the ground substance of the tissue. In addition, the observation that the major structural alterations observed during serratia keratitis can be reproduced by the bacterial protease supports the idea that the enzyme is involved, at least in part, with the production of severe corneal damage by the bacterium.

摘要

通过大体观察、生化分析以及对受影响组织的电子显微镜检查,比较了实验性粘质沙雷氏菌角膜炎和高纯度粘质沙雷氏菌蛋白酶制剂在兔角膜基质中引起的结构改变。在感染发展过程中以及角膜内注射亚微克量的蛋白酶后,出现了急性炎症、角膜液化性坏死和后弹力层膨出。将不溶性角膜基质组织与细菌或蛋白酶进行体外孵育,导致基质蛋白聚糖基质溶解;然而,未检测到特异性胶原酶活性。对受细菌感染和蛋白酶损伤的角膜进行电子显微镜检查发现,蛋白聚糖基质的钌红染色消失,超微结构正常的胶原纤维分散。因此,我们的研究结果表明,粘质沙雷氏菌角膜炎期间以及注射粘质沙雷氏菌蛋白酶后发生的主要角膜损伤是由组织基质的溶解和丧失引起的。此外,在粘质沙雷氏菌角膜炎期间观察到的主要结构改变可由细菌蛋白酶复制,这一观察结果支持了该酶至少部分参与细菌导致严重角膜损伤的观点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9e9/350798/5afd7da51bef/iai00161-0294-a.jpg

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