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In vitro lung epithelial cell transport and anti-interleukin-8 releasing activity of liposomal ciprofloxacin. | LitMetric

In vitro lung epithelial cell transport and anti-interleukin-8 releasing activity of liposomal ciprofloxacin.

Eur J Pharm Sci

Department of Pharmaceutics, School of Pharmacy, Virginia Commonwealth University, 410 N. 12th Street, Richmond, Virginia, 23298, USA.. Electronic address:

Published: March 2018

AI Article Synopsis

  • Liposomal ciprofloxacin (Lipo-CPFX) was studied for its long-acting potential compared to traditional ciprofloxacin (CPFX) using a human lung cell model, focusing on transport and anti-inflammatory effects.
  • The study found that Lipo-CPFX had a 15-times slower transport rate and a 5-times lower uptake in lung cells than CPFX, suggesting it works through a lipid bilayer fusion mechanism.
  • Additionally, both formulations effectively inhibited interleukin-8 (IL-8) release, but Lipo-CPFX maintained this effect even after 24 hours, highlighting its potential for sustained treatment.

Article Abstract

As a promising long-acting inhaled formulation, liposomal ciprofloxacin (Lipo-CPFX) was characterized in the in vitro human lung epithelial Calu-3 cell monolayer system, compared to ciprofloxacin in solution (CPFX). Its modulated absorptive transport and uptake, and sustained inhibitory activity against induced pro-inflammatory interleukin-8 (IL-8) release were examined. The absorptive transport and uptake kinetics for Lipo-CPFX and CPFX were determined at 0.1-50 mg/ml in the Transwell system. The Lipo-CPFX transport was then challenged for mechanistic exploration via cell energy depletion, a reduced temperature, endocytosis and/or lipid fusion inhibition, and addition of excess non-loaded liposomes. The inhibitory activities of Lipo-CPFX and CPFX against lipopolysaccharide (LPS)-induced IL-8 release were assessed in a co-incubation or pre-incubation mode. In the tight Calu-3 cell monolayers, Lipo-CPFX yielded 15-times slower ciprofloxacin flux of absorptive transport and 5-times lower cellular drug uptake than CPFX. Its transport appeared to be transcellular; kinetically linear, proportional to encapsulated ciprofloxacin concentration; and consistent with the cell energy-independent lipid bilayer fusion mechanism. Lipo-CPFX was equipotent to CPFX in the anti-IL-8 releasing activity upon 24 h co-incubation with LPS. Additionally, Lipo-CPFX, but not CPFX, retained the anti-IL-8 releasing activity even 24 h after pre-incubation. In conclusion, Lipo-CPFX enabled slower absorptive lung epithelial cell transport and uptake of ciprofloxacin, apparently via the lipid bilayer fusion mechanism, and the sustained inhibitory activity against LPS-induced IL-8 release, compared to CPFX.

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Source
http://dx.doi.org/10.1016/j.ejps.2018.01.018DOI Listing

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