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首页> 外文期刊>Infection and immunity >Rabbit corneal damage produced by Pseudomonas aeruginosa infection.
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Rabbit corneal damage produced by Pseudomonas aeruginosa infection.

机译：铜绿假单胞菌感染产生的兔角膜损伤。

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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.
机译：对实验性铜绿假单胞菌感染产生的兔角膜破坏的肉眼，光学显微镜和电子显微镜检查显示，急性炎症和角膜液化坏死结合在一起。最初发生上皮细胞的变性和角膜多形核白细胞浸润的开始。这些变化之后是上皮的丧失，角膜细胞和内皮的变性和丧失，蛋白多糖基物质的特征性网状图案的丧失，超微结构正常胶原纤维的散布，大量积累，随后多形核白细胞的退化以及坏死角膜中的血浆蛋白和纤维蛋白。角膜的组织化学检查提示蛋白多糖磨碎的物质丢失了，但胶原蛋白没有丢失。注射溶组织梭状芽孢杆菌胶原酶的兔角膜显示出总体和细胞变化，类似于在假单胞菌感染期间观察到的变化。然而，组织化学检查提示胶原蛋白丢失，电子显微镜检查显示超微结构异常的胶原蛋白原纤维。结果支持这样的想法：（i）铜绿假单胞菌角膜感染期间广泛的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大量的角膜基质而严重破坏角膜。角膜水肿并通过引起角膜蛋白聚糖磨碎的物质的损失，从而导致未受损的胶原纤维的散布，角膜的变弱，以及随后的前房腔压力形成角膜穿孔和角膜穿孔。

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