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暴露应激在单纯疱疹病毒-1感染的受体中诱导可逆性角膜移植混浊。

Exposure Stress Induces Reversible Corneal Graft Opacity in Recipients With Herpes Simplex Virus-1 Infections.

作者信息

Rowe Alexander M, Yun Hongmin, Hendricks Robert L

机构信息

University of Pittsburgh Department of Ophthalmology, Pittsburgh, Pennsylvania, United States.

University of Pittsburgh Department of Immunology, and Microbiology and Molecular Genetics, Pittsburgh, Pennsylvania, United States.

出版信息

Invest Ophthalmol Vis Sci. 2017 Jan 1;58(1):35-41. doi: 10.1167/iovs.16-19673.

DOI:10.1167/iovs.16-19673
PMID:28055100
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5225994/
Abstract

PURPOSE

Most of the inflammation in murine herpes simplex virus type 1 (HSV-1)-induced stromal keratitis (HSK) is due to exposure stress resulting from loss of corneal nerves and blink reflex. Corneal grafts often fail when placed on corneal beds with a history of HSK. We asked if corneal exposure contributes to the severe pathology of corneal grafts on HSV-1-infected corneal beds.

METHODS

Herpes simplex virus type 1-infected corneas were tested for blink reflex. Opacity and vascularization were monitored in allogeneic and syngeneic corneal grafts that were transplanted to corneal beds with no blink reflex or to those that retained blink reflex in at least one quadrant following infection.

RESULTS

Retention of any level of blink reflex significantly reduced inflammation in HSV-1-infected corneas. Corneal allografts placed on HSV-1-infected beds lacking corneal blink reflex developed opacity faster and more frequently than those placed on infected beds that partially or completely retained blink reflex. Corneal grafts placed on infected corneal beds with no blink reflex rapidly became opaque to a level that would be considered rejection. However, protecting these grafts from exposure by tarsorrhaphy prevented or reversed the opacity in both syngeneic and allogenic grafts.

CONCLUSIONS

Exposure due to HSV-1-engendered hypoesthesia causes rapid, severe, persistent, but reversible opacification of both allogeneic and syngeneic corneal grafts. This opacity should not be interpreted as immunologic rejection. Exposure stress may contribute to the high rate of corneal graft pathology in patients with recurrent HSK.

摘要

目的

在小鼠1型单纯疱疹病毒(HSV-1)诱导的基质性角膜炎(HSK)中,大部分炎症是由于角膜神经丧失和眨眼反射导致的暴露应激所致。当角膜移植片置于有HSK病史的角膜床上时,常常会失败。我们研究了角膜暴露是否会导致HSV-1感染的角膜床上角膜移植片出现严重病变。

方法

检测HSV-1感染的角膜的眨眼反射。监测同种异体和同基因角膜移植片的混浊和血管化情况,这些移植片被移植到无眨眼反射的角膜床上,或移植到感染后至少一个象限仍保留眨眼反射的角膜床上。

结果

任何水平的眨眼反射保留均能显著减轻HSV-1感染角膜的炎症。置于缺乏角膜眨眼反射的HSV-1感染角膜床上的角膜同种异体移植片比置于部分或完全保留眨眼反射的感染角膜床上的移植片更快且更频繁地出现混浊。置于无眨眼反射的感染角膜床上的角膜移植片迅速变得混浊至可被视为排斥的程度。然而,通过睑裂缝合术保护这些移植片免受暴露可预防或逆转同基因和同种异体移植片的混浊。

结论

HSV-1引起的感觉减退导致的暴露会使同种异体和同基因角膜移植片迅速、严重、持续但可逆地混浊。这种混浊不应被解释为免疫排斥。暴露应激可能导致复发性HSK患者角膜移植病变的高发生率。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c57d/5225994/6d9eecea60b5/i1552-5783-58-1-35-f03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c57d/5225994/da345e27ab02/i1552-5783-58-1-35-f01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c57d/5225994/0dbb731d8cae/i1552-5783-58-1-35-f02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c57d/5225994/6d9eecea60b5/i1552-5783-58-1-35-f03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c57d/5225994/da345e27ab02/i1552-5783-58-1-35-f01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c57d/5225994/0dbb731d8cae/i1552-5783-58-1-35-f02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c57d/5225994/6d9eecea60b5/i1552-5783-58-1-35-f03.jpg

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2
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Invest Ophthalmol Vis Sci. 2016 Apr;57(4):1578-87. doi: 10.1167/iovs.15-17894.
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Dot1l 通过 p38 MAPK 介导的氧化应激加重小鼠单纯疱疹病毒 1 型诱导的角膜炎。
Oxid Med Cell Longev. 2021 Feb 15;2021:6612689. doi: 10.1155/2021/6612689. eCollection 2021.
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Loss of Osteopontin Expression Reduces HSV-1-Induced Corneal Opacity.骨桥蛋白表达缺失可减少 HSV-1 诱导的角膜混浊。
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