Levofloxacin

Microglia are the main immune cells in the central nervous system. Their excessive activation leads to the release of pro-inflammatory factors (such as IL-1β, TNF-α), causing nerve damage and neuroinflammation. The TLR4/NF-κB signaling pathway is the core pathway for LPS-induced inflammation in microglia.
Levofloxacin can bind to the TLR4–MD-2 complex and exert anti-inflammatory effects by regulating the TLR4/NF-κB pathway. This study provides a theoretical basis for the potential application of Levofloxacin in central nervous system inflammatory-related diseases.
Levofloxacin has no cytotoxicity to microglia within the concentration range of 50–150 μg/mL. The mechanism of its anti-neuroinflammatory effect is:
• Inhibiting the binding of LPS to the TLR4–MD-2 complex
• Preventing TLR4 dimerization
• Inhibiting NF-κB activation and nuclear translocation
• Reducing the release of pro-inflammatory factors such as IL-1β and TNF-α

Fig. 1 Levofloxacin (LVFX) attenuates microglia inflammatory response via TLR4/NF-kB pathway. (Zusso M.; et al. 2019)

Yang Y et al. used a Levofloxacin-loaded porcine acellular dermal matrix (PADM) hydrogel (Lev@PADM) to treat bacterial cystitis. The antibacterial activity, biocompatibility, and immune-modulating capacity of Lev@PADM were investigated both in vitro and in vivo in a mouse UTI model. The PADM hydrogel can release drugs locally and sustainably via intravesical injection. This can increase the concentration of Levofloxacin at the site of infection while reducing potential side effects on the whole body. Compared with oral administration of Levofloxacin, Lev@PADM had long-lasting antibacterial activity, less E. coli invasion, alleviated inflammation by inhibiting NF-κB pathway activation, and maintained the integrity of the gut microbiota.

Fig. 2 Levofloxacin-loaded porcine acellular dermal matrix hydrogel. (Yang Y.; et al. 2024)