TLR2/MyD88/NF-kappa B signaling pathway regulates IL-1 beta production in DF-1 cells exposed to Mycoplasma gallisepticum LAMPs

文献类型: 外文期刊

第一作者: Yu, Ying

作者: Yu, Ying;Chen, Ying;Li, Yuan;Zhang, Lin;Xin, Jiuqing;Chen, Ying;Wang, Yang

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关键词: M. gallisepticum-Derived LAMPs; NF-kappa B; IL-1 beta

期刊名称:MICROBIAL PATHOGENESIS ( 影响因子:3.738; 五年影响因子:3.663 )

ISSN: 0882-4010

年卷期: 2018 年 117 卷

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收录情况: SCI

摘要: Mycoplasma gallisepticum (M. gallisepticum) is one of the most important pathogens that cause chronic respiratory disease in chickens. M. gallisepticum-derived lipid-associated membrane proteins (LAMPs) are thought to be one of the major factors in mycoplasma pathogenesis and are potent inducers of the host innate immune response. However, the interaction of pathogenic M. gallisepticum-derived LAMPs with Toll-like receptors (TLRs) and the signaling pathways responsible for activating inflammation and NF-kappa B have not been fully elucidated. In this study, we found that IL-1 beta expression was induced in DF-1 cells stimulated with M. gallisepticum LAMPs. Subcellular localization experiments using immunofluorescence assays (IFAs) showed p65 translocation from the cytoplasm to the nucleus in DF-1 cells following stimulation with M. gallisepticum LAMPs. Phosphorylation of p65 was detected in LAMP-stimulated DF-1 cells. Treatment with an NF-kappa B-specific inhibitor showed that NF-kappa B is required for M. gallisepticum LAMP-induced IL-1 beta expression. In addition, the results indicated that TLR2 and myeloid differentiation primary-response protein 88 (MyD88)-dependent signaling pathways were involved in the activation of NF-kappa B by M. gallisepticum LAMPs. Together, these results provide evidence that M. gallisepticum LAMPs activate IL-1 beta production through the NF-kappa B pathway via TLR2 and MyD88.

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