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Fig. 6 | Journal of Neuroinflammation

Fig. 6

From: Ciprofloxacin and levofloxacin attenuate microglia inflammatory response via TLR4/NF-kB pathway

Fig. 6

Model depicting cascade of the anti-inflammatory effect of ciprofloxacin and levofloxacin, targeting TLR4–MD-2 complex. LBP facilitates transfer of LPS monomers to CD14, which subsequently shifts the endotoxin to TLR4/MD-2 complex, then leading to formation of TLR4/MD2/LPS ternary complex and its subsequently dimerization. Dimerization of the receptor complex induces the activation of intracellular signaling pathways that involve NF-κB activation and lead to production of pro-inflammatory cytokines (left panel). Fluoroquinolones, such as CPFX and LVFX, exert anti-inflammatory activity, through the inhibition of TLR4/MD2/LPS ternary complex formation, receptor dimerization, and NF-κB nuclear translocation (depicted in light colors in the right panel), resulting in a decreased production of pro-inflammatory cytokines. CD14 cluster of differentiation 14, CPFX ciprofloxacin, IL- interleukin-1 β, LBP LPS binding protein, LPS lipopolysaccharide, LVFX levofloxacin, MD-2 myeloid differentiation protein-2, TLR4 Toll-like receptor 4, TNF-α tumor necrosis factor-α

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