TLR4 overexpression enhances saturated fatty acid-induced inflammatory cytokine gene expression in sheep
文献类型: 外文期刊
作者: Xu, Xue 1 ; Qi, Mei-Yu 3 ; Liu, Shuang 1 ; Song, Xu-Ting 1 ; Zhang, Jia-Nan 1 ; Zhai, Yu-Fei 1 ; Lu, Ming-Hai 4 ; Han, Ho 1 ;
作者机构: 1.Educ Dept Heilongjiang Prov, Key Lab Anim Genet Breeding & Reprod, Harbin, Heilongjiang, Peoples R China
2.Northeast Agr Univ, Coll Anim Sci & Technol, Harbin 150030, Heilongjiang, Peoples R China
3.Heilongjiang Acad Agr Sci, Inst Anim Husb, Harbin, Heilongjiang, Peoples R China
4.Heilongjiang State Farms Sci Technol Vocat Coll, Dept Anim Sci, Harbin, Heilongjiang, Peoples R China
5.China Agr Univ, Beijing Key Lab Anim Genet Improvement, Beijing, Peoples R China
关键词: genetically modified sheep; inflammatory cytokine; saturated fatty acids; Toll-like receptor 4
期刊名称:EUROPEAN JOURNAL OF INFLAMMATION ( 影响因子:0.466; 五年影响因子:0.599 )
ISSN: 2058-7392
年卷期: 2018 年 16 卷
页码:
收录情况: SCI
摘要: Saturated fatty acids (SFAs) can directly stimulate innate immune responses, thereby exacerbating inflammatory aspects of metabolic syndrome. Dietary SFAs act as ligands of Toll-like receptor 4 (TLR4), triggering associated signaling pathways. In this study, we investigated the role of TLR4 in palm oil SFA-associated inflammatory cytokine gene expression in monocytes/macrophages and adipose tissue using TLR4-overexpressing genetically modified sheep. SFA stimulation resulted in upregulation of interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), interleukin-8 (IL-8), interferon-gamma (IFN-gamma), and interleukin-10 (IL-10), and TLR4 overexpression enhanced such SFA-induced inflammatory cytokine expression. Moreover, SFAs markedly activated MyD88-dependent signaling, including IL-1 receptor-associated kinase 4 (IRAK4), TNF receptor-associated factor 6 (TRAF6), and nuclear factor-kappa B (NF-kappa B). Taken together, our results indicate that TLR4 overexpression enhances the SFA-induced inflammatory response through MyD88-dependent signaling in monocytes/macrophages and adipose tissue.
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