Ahn Sang-Ii, Kim Ji-Soo, Hong Chae-Yeon, Gu Gyo-Jeong, Shin Hyeon-Myeong, Jeong Hyun Jung, Koh Kwang Oh, Mang Joo Yang, Kim Dae Young, Youn Hyung-Sun
a Department of Medical Science , College of Medical Sciences, SoonChunHyang University , Asan-Si , Chungnam , Republic of Korea.
b Department of Biomedical Laboratory Science , College of Medical Sciences, SoonChunHyang University , Asan-Si , Chungnam , Republic of Korea.
J Immunoassay Immunochem. 2016;37(3):307-15. doi: 10.1080/15321819.2015.1135162.
Toll-like receptor 4 (TLR4) recognizes LPS and triggers the activation of the myeloid differential factor 88 (MyD88)- and toll-interleukin-1 receptor domain-containing adapter, inducing interferon-β (TRIF)-dependent major downstream signaling pathways. Previously, we presented biochemical evidence that 1-[4-Fluoro-2-(2-nitrovinyl)phenyl]pyrrolidine (FPP), which was synthesized in our laboratory, inhibits NF-κB activation induced by LPS. Here, we investigated whether FPP modulates the TLR4 downstream signaling pathways and what anti-inflammatory target in TLR4 signaling is regulated by FPP. FPP inhibited LPS-induced NF-κB activation by targeting TLR4 dimerization. These results suggest that FPP can modulate the TLR4 signaling pathway at the receptor level to decrease inflammatory gene expression.
