**Figure 8.** Fig. 5 Effects of ciprofloxacin and levofloxacin on LPS binding and LPS-induced TLR4 dimerization. Ba/F3 cells expressing TLR4-Flag (TLR4-F), TLR4-GFP (TLR4-G), MD2-Flag, and CD14 were pretreated with 500 μg/ml ciprofloxacin (CPFX) or levofloxacin (LVFX) for 1 h and then stimulated with 250 ng/ml of a biotinylated LPS (bLPS) or c LPS for 30 min. Cell lysates were immunoprecipitated with mouse anti-GFP antibody. The immunoblotted proteins were exposed to a streptavidin-HRP (upper) or chicken anti-GFP antibody (lower), and the ratio of Biotin-LPS/TLR4-GFP is shown in (b); c mouse anti-Flag (upper) or chicken anti-GFP (lower) antibodies and the ratio of TLR4-Flag/TLR4-GFP is shown in (d). Experiments were performed five times and representative images are shown. Data, expressed as percentage of LPS-stimulated cells, are shown as means ± SEM (n = 5). Data were analyzed by Kruskal-Wallis test (p = 0.0021) followed by Dunn’s multiple comparison test. *p < 0.05 and **p < 0.01 versus LPS stimulation. bLPS biotinylated LPS, Bio biotin, IP immunoprecipitation, IB immunoblot, Veh vehicle

Açıklama

LPS binding and TLR4 dimerization assays in Ba/F3 cells demonstrate that fluoroquinolones interfere with the initial receptor activation step of innate immune signaling.

More Figures from This Paper

Figure 4

Molecular docking analysis reveals two alternative binding conformations of ciprofloxacin within the TLR4-MD-2 complex binding pocket, suggesting direct physical interaction with the innate immune receptor.

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Figure 5

Cell viability assays demonstrate that ciprofloxacin and levofloxacin at the tested concentrations do not significantly reduce microglial survival, confirming that anti-inflammatory effects are not due to cytotoxicity.

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Figure 6

Cytokine release profiles from LPS-stimulated cortical microglia reveal dose-dependent reductions in TNF-alpha and IL-6 following fluoroquinolone treatment.

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Figure 7

NF-kB nuclear translocation in LPS-stimulated microglia is attenuated by both ciprofloxacin and levofloxacin, as shown by immunofluorescence or reporter gene assays.

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Figure 9

Proposed mechanistic model depicts how ciprofloxacin and levofloxacin target the TLR4-MD-2 complex to block LPS-induced downstream signaling cascades and cytokine production.

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Figure 8

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Source Paper

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

Journal of neuroinflammation (2019)

PMID: 31319868

DOI: 10.1186/s12974-019-1538-9

Cite This Figure

![Figure 8: LPS binding and TLR4 dimerization assays in Ba/F3 cells demonstrate that fluoroquinolones interfere with the initial receptor activation step of innate immune signaling.](https://pdfs.citedhealth.com/figures/31319868/112.png)

> Source: Morena Zusso et al. "Ciprofloxacin and levofloxacin attenuate microglia inflammatory response via TLR." *Journal of neuroinflammation*, 2019. PMID: [31319868](https://pubmed.ncbi.nlm.nih.gov/31319868/)

<figure>
  <img src="https://pdfs.citedhealth.com/figures/31319868/112.png" alt="LPS binding and TLR4 dimerization assays in Ba/F3 cells demonstrate that fluoroquinolones interfere with the initial receptor activation step of innate immune signaling." />
  <figcaption>Figure 8. LPS binding and TLR4 dimerization assays in Ba/F3 cells demonstrate that fluoroquinolones interfere with the initial receptor activation step of innate immune signaling.<br>  Source: Morena Zusso et al. "Ciprofloxacin and levofloxacin attenuate microglia inflammatory response via TLR." <em>Journal of neuroinflammation</em>, 2019. PMID: <a href="https://pubmed.ncbi.nlm.nih.gov/31319868/">31319868</a></figcaption>
</figure>

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