Transcriptomic analyses and experimental verification reveal potential biomarkers and biological pathways of urinary tract infection

转录组分析和实验验证揭示了泌尿道感染的潜在生物标志物和生物学通路

阅读:1

Abstract

Urinary tract infection (UTI) is a common infectious disease. Urinary tract pathogenic Escherichia coli (UPEC) is the main cause of UTIs. At present, antibiotics are mainly used for the treatment of UTIs. However, with the increase of drug resistance, the course of the disease is prolonged. Therefore, identifying the receptors and signal pathways of host cells and tissues will further our understanding of the pathogenesis of UTIs and help in the development of new drug treatments. We used two public microarray datasets (GSE43790, GSE124917) in the Gene Expression Omnibus (GEO) database to identify differentially expressed genes (DEGs) between UTI and normal cell samples. A functional analysis based on Gene Ontology (GO) data, a pathway enrichment analysis based on Kyoto Encyclopedia of Genes and Genomes (KEGG) data and a protein-protein interaction analysis identified the main potential biomarkers and verified them in animal tissues. A total of 147 up-regulated genes and 40 down-regulated genes were identified. GO enrichment analysis showed that these functional changes relate to the terms response to lipopolysaccharide, regulation of cytokine production, and regulation of the inflammatory response. KEGG analysis indicated that urinary tract infections likely involve the TNF-αsignaling pathways. The 20 hub genes were selected from the protein-protein interaction network, and the highly significant hub genes were verified by animal experiments. Our findings provide potential targets for exploring new treatments for urinary tract infections. After a comprehensive analysis of the GEO database, these results may facilitate development of new diagnosis and treatment strategies for urinary tract infections.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。