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)-κB function downstream of BLT2 in this response. These results suggest that a TLR4-MyD88-BLT2-Nox1-ROS-NF-κB pathway contributes to the synthesis of IL-6 in LPS-stimulated mouse macrophages.
| Original language | English |
|---|---|
| Pages (from-to) | e156 |
| Journal | Experimental and Molecular Medicine |
| Volume | 47 |
| DOIs | |
| Publication status | Published - 2015 |
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ASJC Scopus subject areas
- Medicine(all)
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MyD88-BLT2-dependent cascade contributes to LPS-induced interleukin-6 production in mouse macrophage. / Lee, A. Jin; Cho, Kyung Jin; Kim, Jae-Hong.
In: Experimental and Molecular Medicine, Vol. 47, 2015, p. e156.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - MyD88-BLT2-dependent cascade contributes to LPS-induced interleukin-6 production in mouse macrophage
AU - Lee, A. Jin
AU - Cho, Kyung Jin
AU - Kim, Jae-Hong
PY - 2015
Y1 - 2015
N2 - 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)-κB function downstream of BLT2 in this response. These results suggest that a TLR4-MyD88-BLT2-Nox1-ROS-NF-κB pathway contributes to the synthesis of IL-6 in LPS-stimulated mouse macrophages.
AB - 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)-κB function downstream of BLT2 in this response. These results suggest that a TLR4-MyD88-BLT2-Nox1-ROS-NF-κB pathway contributes to the synthesis of IL-6 in LPS-stimulated mouse macrophages.
UR - http://www.scopus.com/inward/record.url?scp=84965183971&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84965183971&partnerID=8YFLogxK
U2 - 10.1038/emm.2015.8
DO - 10.1038/emm.2015.8
M3 - Article
VL - 47
SP - e156
JO - Experimental and Molecular Medicine
JF - Experimental and Molecular Medicine
SN - 1226-3613
ER -