杀白细胞素ED在金黄色葡萄球菌眼内炎发病机制中的作用

Contribution of Leukocidin ED to the Pathogenesis of Staphylococcus aureus Endophthalmitis.

作者信息

Longoria-Gonzalez Luis, Coburn Phillip S, Astley Roger, Chen Yan, Callegan Michelle C

机构信息

Department of Microbiology and Immunology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, United States.

Department of Ophthalmology, Dean McGee Eye Institute, Oklahoma City, Oklahoma, United States.

出版信息

Invest Ophthalmol Vis Sci. 2025 May 1;66(5):11. doi: 10.1167/iovs.66.5.11.

DOI:10.1167/iovs.66.5.11

PMID:40323270

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12060071/

Abstract

PURPOSE

To test the hypothesis that leukocidin ED (LukED) contributes to the pathogenesis of experimental Staphylococcus aureus endophthalmitis.

METHODS

Growth curves were generated for S. aureus strain JE2 and strain JE2 lukE::Tn, the transposon mutant of LukED, in brain heart infusion (BHI) and explanted rabbit vitreous. The expression of leukotoxins (lukSF-PV, lukED, hlgABC, and lukGH) was assessed in 18-hour overnight cultures in BHI, tryptic soy broth, and vitreous. S. aureus endophthalmitis was induced by intravitreal injection of 5000 colony-forming units of JE2 or JE2 lukE::Tn into C57BL/6J mice. At 6, 12, and 24 hours after infection, eyes were assessed for retinal function, intraocular colony-forming units and inflammation, and neutrophil infiltration by flow cytometry. RNA was isolated from infected eyes to assess leukotoxin expression.

RESULTS

Strains JE2 and JE2 lukE::Tn grew similarly in BHI and vitreous. Transcript levels of leukotoxin subunits were lower in vitreous compared with laboratory media. In vivo, no differences in retinal function, intraocular growth, intraocular inflation, or neutrophil infiltration were observed in eyes infected with JE2 or JE2 lukE::Tn. During infection, other leukotoxins were expressed in vivo in the absence of LukED.

CONCLUSIONS

LukED does not seem to be essential for the pathogenesis of experimental S. aureus endophthalmitis. However, other leukotoxins are expressed in vivo, which may compensate for the effects of LukED during infection.

摘要

目的

检验杀白细胞素ED（LukED）促成实验性金黄色葡萄球菌眼内炎发病机制的这一假说。

方法

生成金黄色葡萄球菌JE2菌株及其LukED转座子突变体JE2 lukE::Tn在脑心浸液（BHI）和离体兔玻璃体内的生长曲线。在BHI、胰蛋白胨大豆肉汤和玻璃体内的18小时过夜培养物中评估白细胞毒素（lukSF-PV、LukED、hlgABC和lukGH）的表达。通过向C57BL/6J小鼠玻璃体内注射5000个JE2或JE2 lukE::Tn的菌落形成单位来诱导金黄色葡萄球菌眼内炎。在感染后6、12和24小时，评估眼睛的视网膜功能、眼内菌落形成单位和炎症，以及通过流式细胞术检测中性粒细胞浸润情况。从感染的眼睛中分离RNA以评估白细胞毒素的表达。

结果

JE2和JE2 lukE::Tn菌株在BHI和玻璃体内的生长情况相似。与实验室培养基相比，玻璃体内白细胞毒素亚基的转录水平较低。在体内，感染JE2或JE2 lukE::Tn的眼睛在视网膜功能、眼内生长、眼内炎症或中性粒细胞浸润方面未观察到差异。在感染期间，在没有LukED的情况下，其他白细胞毒素在体内表达。