期刊
EXPERIMENTAL AND MOLECULAR MEDICINE
卷 47, 期 -, 页码 -出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/emm.2015.8
关键词
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资金
- Bio & Medical Technology Development Program [2012M3A9C5048709]
- Basic Science Research Program through National Research Foundation - Ministry of Science, Information and Communication Technologies (ICT) and Future Planning, Republic of Korea [2012R1A2A2A01044526]
- National Research and Development Program for Cancer Control Grant, Ministry for Health and Welfare, Republic of Korea [1220020]
- Korea Health Promotion Institute [1220020] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
- National Research Foundation of Korea [2012R1A2A2A01044526] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
Endotoxic responses to bacterial lipopolysaccharide (LPS) are triggered by Toll-like receptor 4 (TLR4) and involve the production of inflammatory mediators, including interleukin-6 (IL-6), by macrophages. The detailed mechanism of IL-6 production by macrophages in response to LPS has remained unclear, however. We now show that LPS induces IL-6 synthesis in mouse peritoneal macrophages via the leukotriene B4 receptor BLT2. Our results suggest that TLR4-MyD88 signaling functions upstream of BLT2 and that the generation of reactive oxygen species (ROS) by NADPH oxidase 1 (Nox1) and consequent activation of the transcription factor nuclear factor (NF)-kappa B function downstream of BLT2 in this response. These results suggest that a TLR4-MyD88-BLT2-Nox1-ROS-NF-kappa B pathway contributes to the synthesis of IL-6 in LPS-stimulated mouse macrophages.
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