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Updated: Jun 13, 2025
Analysis of Protein-protein Interactions and Co-localization Between Components of Gap, Tight, and Adherens Junctions in Murine Mammary Glands
Published on: May 30, 2017
UID-Dual Transcriptome Sequencing Analysis of the Molecular Interactions between Streptococcus agalactiae ATCC 27956
Jishang Gong1,2, Taotao Li1, Yuanfei Li2
1College of Science and Technology, Gansu Agriculture University, Lanzhou 730070, China.
Abstract:
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.
Insights
Streptococcus agalactiae infection disrupts mammary epithelial cell immunity by altering gene expression and splicing. Understanding these molecular interactions is key to developing new mastitis treatments.
Area of Science:
- Microbiology
- Molecular Biology
- Immunology
Background:
- Streptococcus agalactiae causes contagious mastitis, posing treatment challenges due to its high infectivity for mammary epithelial cells.
- The molecular mechanisms underlying S. agalactiae interactions with host mammary epithelial cells are not fully understood.
Purpose of the Study:
- To analyze differential gene expression in mammary epithelial cells during S. agalactiae infection.
- To elucidate the molecular interactions between S. agalactiae and host cells.
Main Methods:
- UID-Dual transcriptome sequencing was employed to analyze host and pathogen gene expression.
- Bioinformatics tools were used to identify differentially expressed genes (DEGs) and enriched pathways.
Main Results:
- Identified 211 differentially expressed host mRNAs and 452 differentially expressed host lncRNAs, enriched in immune and cancer-related pathways.
- Detected 854 differentially expressed pathogen mRNAs, mainly involved in metabolism and biosynthesis.
- Revealed bacterial interference with host alternative splicing, specifically targeting RUNX1 and BCL2L11 via bacterial genes tsf, prfB, and infC.
Conclusions:
- S. agalactiae disrupts host innate immunity by interfering with alternative splicing pathways.
- Host cells activate pathways like ERK1/2 to produce reactive oxygen species (ROS) against bacteria.
- Bacterial interference with host gene regulation highlights a novel virulence mechanism in mastitis pathogenesis.
