葡萄球菌和链球菌性眼内炎中细胞因子的表达。

Biomedicine Hub Pub Date : 2022-07-04 eCollection Date: 2022-05-01 DOI:10.1159/000525330
Marcus Y Soon, Penelope J Allen, Rosie C H Dawkins
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引用次数: 2

摘要

背景:眼内炎是一种眼部组织感染,通常会对视力造成毁灭性的影响。免疫调节是眼内炎治疗干预的新兴途径,细胞因子的表达是潜在机制的核心。本文以系统的方法回顾了动物和人类葡萄球菌和链球菌性眼内炎中细胞因子的表达。方法和结果:检索了四个在线数据库,以研究葡萄球菌和/或链球菌性眼内炎动物模型或人群的细胞因子水平。在确定的1060篇文章中,本综述包括14项研究,包括8种动物模型和6种人类群体。金黄色葡萄球菌、表皮葡萄球菌和肺炎链球菌眼内炎小鼠、大鼠和家兔模型IL-1β、IL-6、IFN-γ、TNF-α和IL-8水平均升高,且在表皮葡萄球菌感染时出现较早的峰值。与对照组相比,人眼内炎表现出一系列促炎和抗炎细胞因子、趋化因子和生长因子的中介水平显著增加。在细胞因子浓度与初始视力和视力预后之间建立了一些关联,但各试验之间没有一致的相关性。结论:可能是毒力因子和toll样受体的联合激活影响了眼内炎的病原体特异性视力结果。此外,疾病的严重程度和潜在的治疗靶点可能取决于协同和代偿细胞因子途径以及抗炎介质的表达。未来的研究应旨在更好地描述炎症介质的作用,并巩固病原体、炎症和眼内炎结局之间的联系。这对临床预防和治疗眼内炎具有激动人心的意义。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Cytokine Expression in Staphylococcal and Streptococcal Endophthalmitis.

Background: Endophthalmitis is an infection of ocular tissues, often with devastating outcomes for vision. Immunomodulation is an emerging avenue for therapeutic intervention in endophthalmitis, with the expression of cytokines central to potential mechanisms. This literature review with a systematic approach characterizes the cytokine expression in both animal and human staphylococcal and streptococcal endophthalmitis.

Method and results: Four online databases were searched for studies profiling cytokine levels in animal models or human populations with staphylococcal and/or streptococcal endophthalmitis. Of the 1,060 articles identified, 14 studies were included in this review comprising eight animal models and six human populations. Mouse, rat, and rabbit models of Staphylococcus aureus, Staphylococcus epidermidis, and Streptococcus pneumoniae endophthalmitis had elevated levels of IL-1β, IL-6, IFN-γ, TNF-α, and IL-8, with earlier peaks observed in S. epidermidis infection. Human endophthalmitis demonstrated significantly increased mediator levels compared to controls for a range of pro-inflammatory and anti-inflammatory cytokines, chemokines, and growth factors. Several associations were established between cytokine concentrations and both initial visual acuity and visual prognosis, with no consistent correlations across trials.

Conclusions: It may be that virulence factors and the combinations of toll-like receptors activated influence the pathogen-specific visual outcomes observed in endophthalmitis. Furthermore, disease severity and potential therapeutic targets may be dependent on synergistic and compensatory cytokine pathways and the expression of anti-inflammatory mediators. Future research should aim to better characterize the roles of inflammatory mediators and solidify associations between pathogens, inflammation, and endophthalmitis outcomes. This has exciting implications for the prevention and treatment of endophthalmitis in clinical settings.

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