MyD88-BLT2-dependent cascade contributes to LPS-induced interleukin-6 production in mouse macrophage.
- Author:
A Jin LEE
1
;
Kyung Jin CHO
;
Jae Hong KIM
Author Information
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- MeSH: Animals; Cell Line; Interleukin-6/*biosynthesis; Leukotriene B4/metabolism; Ligands; Lipopolysaccharides/immunology; Macrophages/immunology/*metabolism; Macrophages, Peritoneal/immunology/metabolism; Mice; Myeloid Differentiation Factor 88/*metabolism; NADH, NADPH Oxidoreductases/metabolism; NF-kappa B/metabolism; Reactive Oxygen Species/metabolism; Receptors, Leukotriene B4/*metabolism; Signal Transduction
- From:Experimental & Molecular Medicine 2015;47(4):e156-
- CountryRepublic of Korea
- Language:English
- Abstract: 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)-kappaB function downstream of BLT2 in this response. These results suggest that a TLR4-MyD88-BLT2-Nox1-ROS-NF-kappaB pathway contributes to the synthesis of IL-6 in LPS-stimulated mouse macrophages.
