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Gene microarray integrated with iTRAQ-based proteomics for the discovery of NLRP3 in LPS-induced inflammatory response of bovine mammary epithelial cells

文献类型： 外文期刊

作者： Sun, Yu 1 ; Li, Lian 1 ; Li, Chengmin 1 ; Wang, Genlin 1 ; Xing, Guangdong 3 ;

作者机构： 1.Nanjing Agr Univ, Coll Anim Sci & Technol, Nanjing, Peoples R China

2.Henan Agr Univ, Coll Anim Sci & Vet Med, Zhengzhou, Henan, Peoples R China

3.Jiangsu Acad Agr Sci, Inst Anim Sci, Nanjing, Peoples R China

关键词： Bovine mammary epithelial cell; inflammatory response; lipopolysaccharide (LPS); Nod Like Receptor Pyrins-3 (NLRP3)

期刊名称：JOURNAL OF DAIRY RESEARCH （ 影响因子：1.904； 五年影响因子：2.019 ）

ISSN： 0022-0299

年卷期： 2019 年 86 卷 4 期

页码：

收录情况： SCI

摘要： Mastitis, a major infectious disease in dairy cows, is characterized by an inflammatory response to pathogens such as Escherichia coli and Staphylococcus aureus. To better understand the immune and inflammatory response of the mammary gland, we stimulated bovine mammary gland epithelial cells (BMECs) with E. coli-derived lipopolysaccharide (LPS). Using transcriptomic and proteomic analyses, we identified 1019 differentially expressed genes (DEGs, fold change >= 2 and P-value < 0.05) and 340 differentially expressed proteins (DEPs, fold change >= 1.3 and P-value < 0.05), of which 536 genes and 162 proteins were upregulated and 483 genes and 178 proteins were downregulated following exposure to LPS. These differentially expressed genes were associated with 172 biological processes; 15 Gene Ontology terms associated with response to stimulus, 4 associated with immune processes, and 3 associated with inflammatory processes. The DEPs were associated with 51 biological processes; 2 Gene Ontology terms associated with response to stimulus, 1 associated with immune processes, and 2 associated with inflammatory processes. Meanwhile, several pathways involved in mammary inflammation, such as Toll-like receptor, NF-kappa B, and NOD-like receptor signaling pathways were also represented. NLRP3 depletion significantly inhibited the expression of IL-1 beta and PTGS2 by blocking caspase-1 activity in LPS-induced BMECs. These results suggest that NLR signaling pathways works in coordination with TLR4/NF-kappa B signaling pathways via NLRP3-inflammasome activation and pro-inflammatory cytokine secretion in LPS-induced mastitis. The study highlights the function of NLRP3 in an inflammatory microenvironment, making NLRP3 a promising therapeutic target in Escherichia coli mastitis.

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