Deep sequencing-based analysis of gene expression in bovine mammary epithelial cells after Staphylococcus aureus, Escherichia coli, and Klebsiella pneumoniae infection

Abstract

ABSTRACT. The goal of this study was to characterize the transcriptome of primary bovine mammalian epithelial cells (pBMECs) and to identify candidate genes for response and resistance to Staphylococcus aureus (strain S108), Escherichia coli (strain E23), and Klebsiella pneumoniae (strain K96) infection. Using Solexa sequencing, approximately 4.9 million total sequence tags were obtained from each of the three infected libraries and the control library. Gene Ontology (GO) analysis of the S108-infected pBMECs showed differentially expressed genes (DEGs) were significantly involved in metabolic processes. In E23-infected pBMECs, DEGs were predominantly associated with cell death and programmed cell death GO terms, while in K96-infected pBMECs, DEGs were primarily involved in metabolic processes and in utero embryonic development. Analysis of the cluster of orthologous groups of proteins showed that the S108-infected, E23-infected and K96-infected pBMECs were significantly involved in "Translation, ribosomal structure and biogenesis", "General function prediction only" and "Replication, recombination and repair". The transcriptome sequences were also annotated for KEGG orthology, and it was found that DEGs in S108-infected pBMECs were significantly 16949 pBMEC gene expression after mastitis pathogen infection ©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 14 (4): 16948-16965 (2015) involved in oxidative phosphorylation and Parkinson's disease. The clustered pathway terms of the DEGs of the E23-infected pBMECs were found to involve the NOD-like receptor signaling pathway and oxidative phosphorylation, while those of the K96-infected pBMECs were primarily involved in oxidative phosphorylation and apoptosis. Our results have identified a number of immune-related genes that showed changes in gene expression after bacterial infection, and provided insight into the interactions between pBMECs and the bacteria.

Klebsiella pneumoniae infection causes mitochondrial damage and dysfunction in bovine mammary epithelial cells

“…Transcriptome analysis, including GO enrichment analysis and pathway enrichment analysis, was done as a systemic screening of up or down-regulated genes in bMECs after infection with two strains of K. pneumoniae. Whole transcriptome analysis has been used to explore DEGs that may be involved in particular biological processes in bMECs infected by K. pneumoniae [25,26]. In the present study, DEGs associated with mitochondria were the most common DEGs enriched in bMECs after infection with K. pneumoniae, indicating that K. pneumoniae had appreciable impacts on mitochondrial functions.…”

Tea Tree Oil Prevents Mastitis-Associated Inflammation in Lipopolysaccharide-Stimulated Bovine Mammary Epithelial Cells

“…Therefore, we speculate that TTO might alleviate inflammatory responses in BMEC via NF-κB, MAPK4, and caspase-3 signaling pathways. The previous study sequenced the transcriptome of BMEC infected by Staphylococcus aureus, E. coli and Klebsiella pneumoniae using the Solexa system, and GO analysis indicated that the differentially expressed genes in the infected and non-infected groups were enriched in cell metabolism, apoptosis and embryonic development (25). Additionally, cluster analysis of homologous proteins revealed that they participate in translation, ribosome biosynthesis and repair.…”

Bacteriophages isolated from dairy farm mitigated Klebsiella pneumoniae-induced inflammation in bovine mammary epithelial cells cultured in vitro

“…Bovine mammary epithelial cells (bMECs) are the first line of defense against invading pathogens that enter the udder through the streak canal, at the distal end of the bovine teat [4,7]. Thus, bMECs have critical roles in both nonspecific and specific immune defenses against infection by pathogenic microorganisms [7]; furthermore, they can be infected by a variety of pathogenic microorganisms that damage these cells, leading to mastitis [8,9]. Toll-like Receptor 4 (TLR4) and the NF-κB pathway are classic regulators of inflammation [10].…”