UID-Dual Transcriptome Sequencing Analysis of the Molecular Interactions between Streptococcus agalactiae ATCC 27956 and Mammary Epithelial Cells

被引:0
作者
Gong, Jishang [1 ,2 ]
Li, Taotao [1 ]
Li, Yuanfei [2 ]
Xiong, Xinwei [2 ]
Xu, Jiguo [2 ]
Chai, Xuewen [2 ]
Ma, Youji [1 ]
机构
[1] Gansu Agr Univ, Coll Sci & Technol, Lanzhou 730070, Peoples R China
[2] Nanchang Normal Univ, Inst Biol Technol, Nanchang 330030, Peoples R China
关键词
mastitis; Streptococcus agalactiae; UID-Dual; transcriptome sequencing; mammary epithelial cells; STREPTOCOCCUS-AGALACTIAE; EXPRESSION; DETERMINANTS; MASTITIS; SUGGESTS; PROTEIN; UDDER;
D O I
10.3390/ani14172587
中图分类号
S8 [畜牧、 动物医学、狩猎、蚕、蜂];
学科分类号
0905 ;
摘要
Streptococcus agalactiae ATCC 27956 is a highly contagious Gram-positive bacterium that causes mastitis, has a high infectivity for mammary epithelial cells, and becomes challenging to treat. However, the molecular interactions between it and mammary epithelial cells remain poorly understood. This study analyzed differential gene expression in mammary epithelial cells with varying levels of S. agalactiae infection using UID-Dual transcriptome sequencing and bioinformatics tools. This study identified 211 differentially expressed mRNAs (DEmRNAs) and 452 differentially expressed lncRNAs (DElncRNAs) in host cells, primarily enriched in anti-inflammatory responses, immune responses, and cancer-related processes. Additionally, 854 pathogen differentially expressed mRNAs (pDEmRNAs) were identified, mainly enriched in protein metabolism, gene expression, and biosynthesis processes. Mammary epithelial cells activate pathways, such as the ERK1/2 pathway, to produce reactive oxygen species (ROS) to eliminate bacteria. The bacteria disrupt the host's innate immune mechanisms by interfering with the alternative splicing processes of mammary epithelial cells. Specifically, the bacterial genes of tsf, prfB, and infC can interfere with lncRNAs targeting RUNX1 and BCL2L11 in mammary epithelial cells, affecting the alternative splicing of target genes and altering normal molecular regulation.
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页数:23
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