title: Lipopolysaccharide increases Toll-like receptor 4 and downstream Toll-like receptor signaling molecules expression in bovine endometrial epithelial cells.
abstract: The endometrium is easily contaminated with bacteria and the endometrial epithelial cells (EECs) play an important role in defence against invading pathogens which recognized pathogen-associated molecular patterns (PAMPs) via pattern recognition receptors (PRRs). Toll-like receptor 4 (TLR4) can recognize lipopolysaccharide (LPS) from Gram-negative bacteria and initiates innate immune responses. In this study, we stimulated bovine EECs with LPS from Escherichia coli (E. coli). The expression of TLR4 was detected by quantitative real-time polymerase chain reaction (qRT-PCR) and western blot. The expression of downstream TLR4 signaling molecules was detected by qRT-PCR. The results showed that TLR4 and downstream adaptor molecules, transcription factors and cytokines were up-regulated when bovine EECs were stimulated with LPS. Furthermore, the expression of TOLLIP and β-defensin 5 were up-regulated when cells were stimulated with LPS. The results demonstrated that both MyD88 dependent and independent pathways in TLR4 were activated by LPS in bovine EECs. Bovine EECs have the immune repertoires required in defending against E. coli and play an important role in innate immune defence of the bovine endometrium.
authors.affiliation: Department of Clinical Veterinary Medicine, College of Animal Science and Veterinary Medicine, Jilin University, Changchun, Jilin Province 130062, People's Republic of China.
authors.forename: Yunhe
authors.initials: Y
authors.lastname: Fu
authors.forename: Bo
authors.initials: B
authors.lastname: Liu
authors.forename: Xiaosheng
authors.initials: X
authors.lastname: Feng
authors.forename: Zhicheng
authors.initials: Z
authors.lastname: Liu
authors.forename: Dejie
authors.initials: D
authors.lastname: Liang
authors.forename: Fengyang
authors.initials: F
authors.lastname: Li
authors.forename: Depeng
authors.initials: D
authors.lastname: Li
authors.forename: Yongguo
authors.initials: Y
authors.lastname: Cao
authors.forename: Shuang
authors.initials: S
authors.lastname: Feng
authors.forename: Xichen
authors.initials: X
authors.lastname: Zhang
authors.forename: Naisheng
authors.initials: N
authors.lastname: Zhang
authors.forename: Zhengtao
authors.initials: Z
authors.lastname: Yang
mesh_terms: D000818:Animals; D002417:Cattle; D002478:Cells, Cultured; D016207:Cytokines / Q000235:genetics; D004717:Endometrium / Q000187:drug effects* / Q000276:immunology* / Q000382:microbiology; D004847:Epithelial Cells / Q000187:drug effects / Q000276:immunology / Q000382:microbiology; D004926:Escherichia coli / Q000276:immunology / Q000472:pathogenicity; D005260:Female; D007113:Immunity, Innate; D047908:Intracellular Signaling Peptides and Proteins / Q000235:genetics; D008070:Lipopolysaccharides / Q000276:immunology / Q000633:toxicity*; D053594:Myeloid Differentiation Factor 88 / Q000235:genetics; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction; D051195:Toll-Like Receptor 2 / Q000235:genetics / Q000378:metabolism; D051197:Toll-Like Receptor 4 / Q000235:genetics / Q000378:metabolism*; D014157:Transcription Factors / Q000235:genetics; D015854:Up-Regulation / Q000187:drug effects; D023083:beta-Defensins / Q000235:genetics
chemical_list: D016207:Cytokines; D047908:Intracellular Signaling Peptides and Proteins; D008070:Lipopolysaccharides; D053594:Myeloid Differentiation Factor 88; D012333:RNA, Messenger; D051195:Toll-Like Receptor 2; D051197:Toll-Like Receptor 4; D014157:Transcription Factors; D023083:beta-Defensins