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微生物群在绿眼病中的作用

Ling Huang¹, Yiwen Hong¹, Xiangyu Fu¹

¹The Department of Ophthalmology, West China Hospital, Sichuan University, Chengdu, 610041, China; The Research Laboratory of Ophthalmology and Vision Sciences, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, 610041, China.

Molecular aspects of medicine

|October 22, 2023

概括

玻璃眼包括视网膜质细胞的损失. 新兴的研究将肠道微生物群失调和代谢物与玻璃眼病原体联系起来,这表明除了降低眼内压力之外还有新的治疗点.

科学领域:

眼科医生眼科眼科
微生物学微生物学
免疫学免疫学免疫学

背景情况:

玻璃眼是不可逆转的视力丧失的主要原因,原因是视网膜质细胞 (RGC) 和视神经轴突退化.
虽然高眼内压 (IOP) 是一个关键的危险因素,但非IOP途径和诸如衰老,肥胖和抑郁等因素也会导致青光眼的发展.
人类微生物群显著影响健康和疾病,在绿眼病患者的不同位置观察到异位生物.

研究的目的:

审查近期关于青光眼中的微生物群和代谢物变化的发现.
探索失生症在青光眼病原体中的作用,考虑风险因素和潜在的机制.
讨论新兴的治疗策略,以准绿眼病管理的微生物群.

主要方法:

综述过去十年的文献,重点关注微生物群和代谢物变化.
从动物模型,青光眼患者和患有青光眼风险因素 (老龄化,肥胖,抑郁症) 的个人中分析数据.
检查包括抗原仿真,热应激蛋白 (HSP) 透,LPS-TLR4通路和微生物衍生的代谢物在内的拟议机制.

主要成果:

青光眼患者在眼睛,口腔,胃和肠道环境中表现出异位生物.
与RGC损伤有关的机制包括抗原仿真,HSP特异性T细胞透和LPS-TLR4通路.
微生物代谢物和感染 (H. pylori,CMV) 可能通过同型氨酸的积累,炎症和直接传播导致青光眼.

结论:

微生物群失生症通过各种分子机制参与了玻璃眼病原体的产生.
通过抗生素,饮食改变或便移植向微生物群提供了潜在的治疗途径.
需要进一步的研究,以阐明临床应用的失生症和青光眼之间的精确分子联系.

关键词:

16S rRNA 基因测序的基因测序衰老的衰老衰老的衰老抗原仿真是一种仿真.细胞メガロウイルス (CMV)眼光障碍眼光障碍眼光障碍眼光障碍热应激蛋白 (HSP) 是一种热应激蛋白.在Helicobacter Pylori的研究中,眼内压力眼内压力在LPS中使用LPS.微生物群中的微生物群肥胖导致的抑郁症在 TLR4 中,麻疹病毒 (Varicella zoster virus,简称VZV) 是一种流感病毒.

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