Mycoplasma bovis-derived lipid-associated membrane proteins activate IL-1 beta production through the NF-kappa B pathway via toll-like receptor 2 and MyD88
文献类型: 外文期刊
第一作者: Wang, Yang
作者: Wang, Yang;Liu, Suli;Li, Yuan;Wang, Qi;Shao, Jiari;Chen, Ying;Xin, Jiuqing
作者机构:
关键词: Mycoplasma bovis-derived LAMPs;NF-kappa B;IL-1 beta
期刊名称:DEVELOPMENTAL AND COMPARATIVE IMMUNOLOGY ( 影响因子:3.636; 五年影响因子:3.654 )
ISSN: 0145-305X
年卷期: 2016 年 55 卷
页码:
收录情况: SCI
摘要: Mycoplasma bovis causes pneumonia, otitis media, and arthritis in young calves, resulting in economic losses to the cattle industry worldwide. M. bovis pathogenesis results in part from excessive immune responses. Lipid-associated membrane proteins (LAMPs) can potently induce host innate immunity. However, interactions between M. bovis-derived LAMPs and Toll-like receptors (Tilts), or signaling pathways eliciting active inflammation and NF-kappa B activation, are incompletely understood. Here, we found that IL-1 beta expression was induced in embryonic bovine lung (EBL) cells stimulated with M. bovis-derived LAMPs. Subcellular-localization analysis revealed nuclear p65 translocation following EBL cell stimulation with M. bovis-derived LAMPs. An NF-kappa B inhibitor reversed M. bovis-derived LAMP-induced IL-1 beta expression. TLR2 and myeloid differentiation primary response gene 88 (MyD88) overexpression increased LAMP-dependent IL-1 beta induction. TLR2-neutralizing antibodies reduced IL-1 beta expression during LAMP stimulation. LAMPs also inhibited IL-1 beta expression following overexpression of a dominant-negative MyD88 protein. These results suggested that M. bovis-derived LAMPs activate IL-1 beta production through the NF-kappa B pathway via TLR2 and MyD88. (C) 2015 Elsevier Ltd. All rights reserved.
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