Impediment of corneal cell migration by a bacterial factor

细菌因素阻碍角膜细胞迁移

• 批准号: 8904988
• 负责人: Kimberly M Brothers
• 金额: $ 5.42万
• 依托单位: UNIVERSITY OF PITTSBURGH AT PITTSBURGH
• 依托单位国家: 美国
• 财政年份: 2015
• 资助国家: 美国
• 起止时间: 2015-05-01 至 2017-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8904988
• 关键词: American; Bacteria; Basic Science; Biochemical; Biology; Blindness; Cells; Cicatrix; Communication; Contact Lenses; Cornea; Corneal Injury; Defect; Disease; Epithelial; Epithelial Cells; Eye; Eye Infections; Family suidae; Genes; Genetic; Goals; Human; Immune system; Infection; Infection prevention; Inflammation; Keratitis; Lead; Left; Lipopolysaccharides; Microbe; Modeling; Mutation; Oryctolagus cuniculus; Personal Satisfaction; Physiology; Process; Production; Quality of life; Research; Role; Scientist; Serratia marcescens; Syndrome; Testing; Therapeutic; United States; Virus; Vision; Wound Healing; cell motility; corneal scar; driving force; experience; frontier; fungus; human tissue; in vivo; inhibitor/antagonist; insight; microbial; microbiome; mutant; novel; pathogen; prevent; public health relevance; tool

 DESCRIPTION (provided by applicant): Every year in the United States 10% of contact lens wearers experience contact lens associated red eye (CLARE), lowering the quality of life of millions of Americans. A related corneal affliction is microbial keratitis (MK), a potentially blinding disease that has left millions of people with vision loss worldwide. Host-pathogen interactions are a driving force in both afflictions. The ability of corneas to respond to disease s dependent upon our immune system and ability to heal wounds. Microbes (bacteria, fungi, and viruses) have employed numerous mechanisms for manipulating our immune system and basic physiology. Each of us is awash with microbes, yet our understanding of how these microbes communicate with our cells is poorly understood. The long-term goal of this research is to elucidate fundamental host-pathogen communication that is profoundly important for our well-being and instrumental for establishing disease. This study focuses on how a factor(s) secreted by Serratia marcescens inhibits corneal wound-healing by 1) identifying if these bacterial secreted factor(s) prevent wound healing in vivo in a rabbit corneal wound healing model and 2) testing the hypothesis the factor secreted by S. marcescens that inhibits corneal cell migration is lipolysaccharide. These answers may lead to therapeutic strategies for treating ocular infections and reduce infection-associated vision loss.

 描述(申请人提供)：在美国，每年有10%的隐形眼镜佩戴者经历过隐形眼镜相关性红眼(Clare)，降低了数百万美国人的生活质量。一种相关的角膜疾病是微生物性角膜炎(MK)，这是一种潜在的致盲疾病，已导致全球数百万人失明。宿主-病原体的相互作用是这两种疾病的驱动力。角膜对疾病的反应能力S取决于我们的免疫系统和愈合伤口的能力。微生物(细菌、真菌和病毒)已经使用了许多机制来操纵我们的免疫系统和基本生理。我们每个人都有大量的微生物，但我们对这些微生物如何与我们的细胞交流的了解却很少。这项研究的长期目标是阐明基本的宿主-病原体沟通，这对我们的福祉和建立疾病的工具是极其重要的。本研究主要研究粘质沙雷氏菌分泌的一种因子(S)如何通过以下途径抑制角膜创伤愈合：1)确定这些细菌分泌因子(S)是否在兔角膜创伤愈合模型中阻止伤口愈合；2)检验粘质沙雷氏菌分泌的抑制角膜细胞迁移的因子是 脂多糖。这些答案可能导致治疗眼部感染和减少与感染相关的视力损失的治疗策略。