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铜绿假单胞菌感染导致的兔角膜损伤。

Rabbit corneal damage produced by Pseudomonas aeruginosa infection.

作者信息

Gray L D, Kreger A S

出版信息

Infect Immun. 1975 Aug;12(2):419-32. doi: 10.1128/iai.12.2.419-432.1975.

Abstract

Gross, light microscopic, and electron microscopic examination of the rabbit corneal destruction produced by experimental Pseudomonas aeruginosa infections revealed a combination of acute inflammation and liquefaction necrosis of the cornea. Degeneration of the epithelial cells and the start of polymorphonuclear leukocyte infiltration of the cornea occurred initially. These changes were followed by loss of the epithelium, degeneration and loss of the keratocytes and endothelium, loss of the characteristic weblike pattern of the proteoglycan ground substance, dispersal of ultrastructurally normal collagen fibrils, extensive accumulation followed by degeneration of polymorphonuclear leukocytes, and accumulation of plasma proteins and fibrin in the necrotic cornea. Histochemical examination of the cornea suggested a loss of the proteoglycan ground substance but not of collagen. Rabbit corneas injected with Clostridium histolyticum collagenase showed gross and cellular changes similar to those observed during the pseudomonal infections; however, histochemical examination suggested a loss of collagen, and electron microscopy revealed ultrastructurally abnormal collagen fibrils. The results support the idea (i) that a bacterial or host-derived collagenase is not required for extensive corneal damage during a P. aeruginosa corneal infection, and (ii) that a P. aeruginosa corneal infection may severly damage the cornea by producing extensive corneal edema and by causing the loss of the corneal proteoglycan ground substance, thus resulting in dispersal of undamaged collagen fibrils, weakening of the cornea, and subsequent descemetocele formation and corneal perforation by the anterior chamber pressure.

摘要

对实验性铜绿假单胞菌感染所致兔角膜破坏进行大体、光学显微镜和电子显微镜检查,发现角膜呈现急性炎症与液化性坏死并存的情况。最初出现上皮细胞变性以及角膜多形核白细胞浸润。随后发生上皮脱落、角膜细胞和内皮细胞变性及丧失、蛋白聚糖基质特征性网状结构消失、超微结构正常的胶原纤维分散、多形核白细胞大量积聚并变性,以及坏死角膜中血浆蛋白和纤维蛋白积聚。角膜的组织化学检查提示蛋白聚糖基质丧失但胶原未丧失。注射溶组织梭菌胶原酶的兔角膜呈现出与铜绿假单胞菌感染时观察到的类似大体和细胞变化;然而,组织化学检查提示胶原丧失,电子显微镜显示超微结构异常的胶原纤维。这些结果支持以下观点:(i)铜绿假单胞菌角膜感染期间广泛角膜损伤不需要细菌或宿主来源的胶原酶;(ii)铜绿假单胞菌角膜感染可能通过产生广泛角膜水肿和导致角膜蛋白聚糖基质丧失,从而严重损伤角膜,进而导致未受损胶原纤维分散、角膜变薄,随后因前房压力形成后弹力层膨出和角膜穿孔。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/84e0/415299/4d03ccf37df5/iai00236-0197-a.jpg

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